Pharmacognosy Magazine

When the endometrium matures in step with the required morphological changes, blastocyst implantation occurs more effectively.

The present study aimed to examine the reproductive toxicity of apricot kernel oil (AK oil) by using an animal model of early pregnancy in adult BALB/c mice. Materials and Methods: Fifty adult BALB/c mice were first acclimated and then mated. Thirty-two confirmed pregnant mice were allocated into four groups. Monitoring involved recording weight gain and abortion rates, and on gestation day 15 the animals were euthanized for collection of tissue and blood samples. Hematological analysis was performed to evaluate multiple blood indices, while levels of sex hormones and serum inflammatory markers (CRP, IL-6, IL-1β, TNF-α) were measured. Antioxidant capacity, lipid peroxidation, and thiol content in uterine tissue were determined, and gene expression associated with the p53/Cas-3/Bax/Bcl-2 apoptotic pathway was assessed by RT-qPCR.

Exposure to AK oil resulted in significant (p <0.05) decreases in maternal weight gain and placental weight, together with a significant (p <0.05) increase in uterine weight. Hematological findings demonstrated raised WBC and lymphocyte counts, along with significantly reduced (p <0.05) progesterone and estrogen concentrations. Elevated (p <0.05) cytokine levels were observed at the higher AK oil doses. Gene expression analysis showed upregulation (p <0.05) of pro-apoptotic genes and downregulation (p <0.05) of Bcl-2, collectively indicating adverse effects of AK oil on early pregnancy.

Accumulation of AK oil may stimulate the HPG axis and consequently promote reactive oxygen species generation, oxidative stress, mitochondrial apoptosis, and reproductive toxicity.

Allergic rhinitis, a worldwide health issue, is defined by immunoglobulin E (IgE)-mediated inflammation of nasal mucosa, resulting in symptoms like sneezing and nasal obstruction. The increasing incidence of allergic rhinitis globally intensifies the burden on healthcare systems, requiring thorough methods for effective management and prevention.

The current study evaluated the effects of corosolic acid against ovalbumin (OVA)-induced allergic rhinitis in mice.

Allergic rhinitis was triggered in mice with intraperitoneal injection of OVA (1 mg/mL) combined with aluminum hydroxide (20 mg/mL; 0.1 mL/mouse). Corosolic acid was treated at concentrations of 10 and 20 mg/kg, respectively. The analysis of nasal symptoms (nasal rubbings and sneezing) was conducted on the final day of the OVA challenge. The histamine and allergen-specific IgE concentrations in the experimental mice were evaluated utilizing kits. The inflammatory cytokine levels were evaluated in the mice utilizing assay kits.

The treatment of corosolic acid in the OVA-induced mice led to a significant diminution in nasal rubbings and instances of sneezing. In allergic rhinitis-induced mice, corosolic acid treatment effectively reduced the histamine, OVA-specific IgE, and eosinophil infiltration levels. Furthermore, the corosolic acid treatment markedly decreased the inflammatory biomarker levels in the OVA-induced mice with allergic rhinitis.

In conclusion, the current data demonstrated that corosolic acid significantly reduced inflammatory and allergic reactions in OVA-challenged mice. These findings suggest that corosolic acid may be an effective therapeutic agent for treating and preventing allergic rhinitis.

Diabetes mellitus represents a significant health challenge that affects the broader population. A small tree, Commiphora gileadensis (C. gileadensis), is native to the Middle East.

This research investigated the impact of C. gileadensis on blood glucose levels, HbA1c, GLUT2, GLUT4, and lipid profile.

Sixty male mice were divided into six groups: negative control, untreated diabetic, and three groups of diabetic mice treated with C. gileadensis sap, methanolic extract, acetone extract, and the metformin-treated group. Random blood glucose levels, HbA1c, lipid profile, GLUT2, and GLUT4 were assessed for each mouse across the five groups.

The random blood glucose levels, triglycerides, total cholesterol, and HbA1c were markedly decreased in mice administered with C. gileadensis extracts in comparison to the untreated diabetic group. Serum and hepatic GLUT2 were markedly increased in the metformin-treated group compared to untreated diabetic and diabetic treated with C. gileadensis. Serum and muscle GLUT4 levels were elevated in diabetic mice that were administered with the three C. gileadensis extracts relative to the untreated diabetic group.

This study concludes that C. gileadensis sap and its methanol and acetone extracts lower serum random blood glucose levels, HbA1c, and lipid profiles in mice with type 2 diabetes mellitus. Moreover, C. gileadensis extracts may reduce serum random blood glucose levels and HbA1c in diabetic mice via inducing muscle GLUT4.

Ischaemic heart disease (IHD) is currently managed by drugs and minimally invasive procedures. However, the necessity for safe, eco-friendly herbal-based medications is consistently advocated to prevent the side effects. Medicinal plants, rich in cardioprotective phytochemicals, offer promising potential for developing safer therapeutics to mitigate IHD progression while reducing treatment-related risks.

Trans-ferulic acid (TFA), a phenolic secondary metabolite recognised for its various pharmaceutical applications, has been selected for in vitro assessment of its toxicity and cardioprotective efficacy.

H9c2 cells were exposed to ischaemic conditions and treated with varying concentrations of TFA (3.1–50 µg/mL). Cytotoxicity and cardioprotective effects were assessed using MTT and lactate dehydrogenase (LDH) assays. Collagen degradation was evaluated by Sirius Red staining, while quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyse the expression of nuclear factor erythroid 2-related factor 2 (NRF2) and HIF1α genes involved in oxidative stress response and hypoxia regulation.

50 µg/mL TFA showed significantly (p < .001) less toxicity and exhibited 86% viability in ischaemic H9c2 cells; the protective levels were significantly (p < .001) higher (36%) when compared to the untreated group. Decreased LDH activity in the treated group demonstrated the cardioprotective efficacy of TFA, with a value of 239 U/mL compared to the untreated cells (356 U/mL). TFA inhibited the collagen degradation induced by ischaemia, hence preventing the organisation of cardiac muscle tissue, as evidenced by Sirius Red staining. TFA treatment upregulates the NRF2 and suppresses the expression of HIF1α by means of mitigating cellular damage caused by oxidative stress and inflammation, which has a significant impact on the occurrence of IHD.

These findings suggest TFA as a promising phytochemical candidate for developing novel therapeutic strategies against IHD.

Chronic suppurative otitis media (CSOM) is a significant cause of hearing impairment in developing countries and is frequently associated with severe intracranial and extracranial complications. The increasing prevalence of antibiotic-resistant bacterial strains in CSOM cases underscores the urgent requirement for innovative and effective therapeutic strategies. The World Health Organization (WHO) has estimated that approximately 80% of individuals in low-resource countries rely on traditional medicine to satisfy their primary healthcare needs, emphasizing the potential value of plant-based remedies in addressing such infections.

The current study primarily focused on the green synthesis of Reduced graphene oxide–silver nanocomposites (rGO/Ag NCs) using Cleome viscosa leaf extract. Characterization was carried out using various spectroscopic techniques, and anti-microbial activity was evaluated in vitro using the disc diffusion method. The significant role of microbial agents in the etiology of CSOM was underscored by the confirmation of bacterial infections in 79 (61.7%) of the 128 patient-derived samples analyzed. The predominance of drug-resistant strains was revealed through standardized methods for bacterial isolation and identification, underscoring the urgent need for innovative and effective anti-microbial therapies.

The synthesized nanocomposites were characterized using spectroscopic techniques, which showed a consistent dimension of approximately 20 nm and a uniform distribution of AgNPs on graphene sheets, as evidenced by the surface plasmon resonance (SPR) peak at approximately 420 nm. The anti-microbial activity of the rGO/Ag NCs was evaluated using the disc diffusion method, which resulted in inhibition zones measuring 12.85 ± 0 mm for Staphylococcus aureus and 14.08 ± 0 mm for Pseudomonas aeruginosa. The rGO/Ag NCs demonstrated superior anti-bacterial activity against multidrug-resistant microorganisms that are associated with CSOM. Furthermore, the experimental groups did not exhibit any significant differences in body weight, food consumption, or hydration intake, which suggests high biocompatibility and systemic stability.

The rGO/Ag NCs demonstrated effective anti-microbial properties and did not exhibit any signs of acute or subacute toxicity, highlighting their potential as a therapeutic choice for the treatment of CSOM and other associated ear infections.

Cerebral ischemic stroke, a devastating neurological condition, arises from the disruption of blood flow to the brain, resulting in oxygen and nutrient deprivation and subsequent neuronal damage. Ischemic stroke is responsible for a significant number of all stroke incidences, highlighting the urgency for effective treatments.

The present study aimed to investigate the therapeutic efficacy of gigantol in rats with cerebral ischemia–reperfusion injury (CI–RI).

The CI–RI was induced in experimental rats, and gigantol was administered intragastrically at 10 and 20 mg/kg concentrations for 7 days prior to CI–RI induction and for an additional 14 days. The levels of brain edema and infarction in the experimental rats were assessed. The concentrations of antioxidants, oxidative stress markers, inflammatory cytokines, and apoptotic proteins were assessed using the kits.

The current findings demonstrated that gigantol treatment significantly reduced brain edema and infarction levels in CI–RI-induced rats. The gigantol treatment considerably reduced pro-inflammatory cytokine levels and alleviated oxidative stress by enhancing antioxidant concentrations in the brains of CI–RI rats. The gigantol treatment also regulated the levels of apoptotic proteins in the rats with CI–RI.

The current study revealed the neuroprotective effects of gigantol in rats subjected to CI–RI due to its antioxidant, anti-inflammatory, and anti-apoptotic properties. These findings may promote the advancement of gigantol as a potential salutary candidate to treat brain damage due to ischemic stroke.

Nutraceuticals are products being used as food and medicines for the treatment of several chronic diseases. The herbal nutraceuticals are gaining importance because of a wide variety of biological actions due to the presence of phytochemicals, such as alkaloids, glycosides, terpenoids, oils, tannins, and several others, like anthocyanins. These anthocyanins are water-soluble pigments found in plants as secondary metabolites and can be of great therapeutic interest for the management of insulin resistance and non-alcoholic steatohepatitis (NASH).

Mouse intraperitoneal macrophages primed with lipopolysaccharide (LPS, 1 ng/mL) were subjected to treatment with Oryza sativa L. (black rice) and Ipomoea batatas L. (purple sweet potato) extracts. The evaluation focused on assessing the impact of these extracts on the production of inflammatory cytokines (interleukin-6 [IL-6] and tumor necrosis factor alpha [TNF-α]). Additionally, C57Bl/6 mice were kept on a diet deficient in methionine and choline (MCD) for 8 weeks and were administered O. sativa L. (black rice) and I batatas L. (purple sweet potato) to investigate their effects on NASH.

Extracts obtained from O. sativa L. (black rice) and I. batatas L. (purple sweet potato) demonstrated a significant reduction in inflammatory cytokines, as indicated by a marked decline in TNF-α and IL-1β levels in LPS-primed macrophages. Mice on the MCD diet showed NASH phenotype, and treatment with the extracts of black rice and purple sweet potato significantly (p < .05) lowered plasma liver enzyme levels and inflammation, as measured by mRNA analysis, and attenuated fibrosis, as measured by histopathology.

Collectively, the findings of the study validated the hypothesis of O. sativa L. (black rice) and I. batatas L. (purple sweet potato) extract could improve inflammation-associated NASH.

Cadmium is a hepatotoxic heavy metal. Cadmium is known to induce ceramide generation and ferroptosis. Edible insects have recently been touted as a potential functional food. Various studies are being conducted in this regard.

This study was designed to investigate whether two types of insects, Tenebrio molitor larvae (TM) and Protaetia brevitarsis larvae (PB), can inhibit cadmium-induced hepatotoxicity.

TM and PB powder were extracted using 70% ethanol and diluted with phosphate-buffered saline. TM and PB extracts were cotreated with cadmium in Hep3B cells. To investigate the mechanism, desipramine (an acid sphingomyelinase (ASMase) inhibitor), ferrostatin-1 (a ferroptosis inhibitor), and GW4869 (a neutral sphingomyelinase (NSMase) inhibitor) were used with cadmium. Anti-ferroptosis mechanisms of the TM and PB extracts were demonstrated using Western blot, enzyme-linked immunosorbent assay, MTT cell viability assay, real-time polymerase chain reaction analysis, and 2,2′-Azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging assay.

Cadmium increased ceramide generation and ferroptosis, concomitant with increased ASMase and NSMase expressions. To understand which mechanism is the upstream pathway, ferrostatin-1, desipramine, and GW4869 were treated with cadmium. Cadmium-induced hepatotoxicity was partially inhibited by ferrostatin-1, which did not affect ASMase expression and ceramide levels. Desipramine, but not GW4869, reduced cadmium-induced cell death and ferroptosis by reducing ceramide levels. Therefore, ceramide generation by ASMase can be an upstream pathway of ferroptosis in cadmium-induced cell death. Interestingly, TM and PB extracts reduced cadmium-induced ceramide increase and ASMase expression, leading to reduced ferroptosis and cell death. TM and PB extracts also had antioxidant properties due to their ability to scavenge reactive oxygen species.

TM and PB have an anti-ferroptosis mechanism against cadmium, which is due to inhibition of ceramide generation by reducing ASMase expression. Therefore, TM and PB can inhibit cadmium-induced hepatotoxicity as functional foods.

Tanshinone (TSL) is a good traditional Chinese medicine with a wide range of applications. Whether it plays a role in ischemic cerebral infarction is unclear.

This study aims to explore the mechanism of tanshinone (TSL) to improve endoplasmic reticulum stress injury in mice with ischemic cerebral infarction by regulating miR-29 and inhibiting the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.

Ischemic cerebral infarction mouse models were constructed and divided into the NC group, TSL group, TSL+miR-29mimic group, and TSL+miR-29inhibitor group. The expression of P-EIF-2α and P-PERK in the ischemic penumbra cortical area of cerebral infarction lesions was monitored, brain cell apoptosis was observed, and genes related to the miR-29 and PI3K/Akt pathways in the tissue were detected.

A cerebral infarction model was successfully prepared. Compared with the sham operation group, the cerebral infarction site was severely ischemic and larger; TSL had an improved effect on ischemic cerebral infarction, and polydopamine-based nanoparticles (PDA NPs)-TSL had the best effect; TSL can reduce the expression of P-PERK in the cortical area and inhibit the expression of P-EIF-2α in the cortical area of the ischemic penumbra, and TSL has a more significant effect in this aspect. By using agonists and inhibitors of miR-29, TSL promotes the expression of miR-29 and improves endoplasmic reticulum stress injury in mice with ischemic cerebral infarction by inhibiting the PI3K/Akt signaling pathway.

TSL has a good anti-inflammatory effect, can reduce the expression of P-PERK in the cortical area, inhibit the expression of P-EIF-2α in the ischemic penumbra cortical area, and inhibit PI3K/Akt signaling by promoting miR-29 pathway to improve endoplasmic reticulum stress damage in mice with ischemic cerebral infarction.

Thyroid cancer represents the most prevalent endocrine cancer, with papillary thyroid carcinoma responsible for the most cases and presenting a significant clinical challenge due to its variable prognosis.

This work aims to examine the effects of chrysoeriol on thyroid cancer TPC-1 cells, by targeting apoptotic mediators caspase-3, caspase-8, and caspase-9 through molecular docking and evaluating their expression in TPC-1 cells treated with chrysoeriol under in vitro conditions.

The cytotoxic effects of chrysoeriol on the growth of thyroid cancer TPC-1 cells were assessed using an MTT assay. The extent of apoptosis in both untreated and chrysoeriol-treated TPC-1 cells was examined using a dual staining approach. The activity of caspase enzymes (caspase-3, caspase-8, and caspase-9) in untreated and chrysoeriol-exposed TPC-1 cells was assessed using commercial test kits. In addition, the potential interactions of chrysoeriol and doxorubicin (DOX) with the caspase-3, caspase-8, and caspase-9 were evaluated by implementing molecular docking studies.

The treatment of diverse dosages of chrysoeriol effectively inhibited thyroid cancer TPC-1 cells in a dose-dependent manner. Moreover, chrysoeriol treatment markedly increased apoptosis in TPC-1 cells, as demonstrated by the results of the dual staining method. Furthermore, treatment with chrysoeriol also increased the activity of caspase-3, caspase-8, and caspase-9 in thyroid cancer TPC-1 cells. Molecular docking predicted a better interaction of caspase-3 (binding affinity (BA) = −6.7 kcal/mol; RMSD = 1.307Å), caspase-8 (BA = −6.5 kcal/mol; RMSD = 1.709Å), caspase-9 (BA = −6.6 kcal/mol; RMSD = 2.08Å) with the chrysoeriol and caspase-3 (BA = −6.3 kcal/mol; RMSD = 2.757Å), caspase-8 (BA = −6.3 kcal/mol; RMSD = 2.398Å), caspase-9 (BA = −6.7 kcal/mol; RMSD = 2.685Å) with the DOX. These computational results suggest that chrysoeriol may interact well with caspase proteins and contribute to their activation as part of its pro-apoptotic mechanism and caspase activation in thyroid cancer TPC-1 cells.

The present study demonstrates that chrysoeriol exhibits anti-cancer properties against thyroid cancer, inhibiting cell growth and inducing apoptosis in TPC-1 cells by upregulating caspase activity. The increased activities of caspase-3, caspase-8, and caspase-9 indicate that chrysoeriol activates both intrinsic and extrinsic apoptotic pathways. Molecular docking and toxicity analysis further support these findings by revealing better binding affinities between chrysoeriol and the caspase proteins than DOX, suggesting that these interactions may facilitate caspase activation. Thus, the current results highlight that chrysoeriol is a hopeful anti-cancer agent for future thyroid cancer treatment.

Systemic inflammation leading to coronary atherosclerotic heart disease (CAD) increases the risk for Psoriasis (PSO). Despite progress in diagnostic and therapeutic strategies for CAD, it is hard to identify many patients in time, and their lives are threatened.

To explore the comorbidity genes of psoriasis (PSO) and coronary artery disease (CAD) under the intervention of Ustekinumab combined with Astragalus, and to provide new ideas for clinical treatment.

The PSO datasets (GSE13355, GSE14905) and CAD datasets (GSE113079, GSE23561) were obtained from the Gene Expression Omnibus database. Key genes were screened through differential expression analysis, weighted gene co-expression network analysis (WGCNA), gene enrichment analysis, protein–protein interaction (PPI) network construction, and immune infiltration analysis.

A total of 2,412 PSO differential genes and 4,443 CAD differential genes were identified. WGCNA analysis yielded 8,809 PSO-related module genes and 8,389 CAD-related module genes. Cross-analysis identified 186 genes with consistent expression trends. Eventually, aurora kinase B (AURKB), C-X-C motif chemokine ligand 11 (CXCL11), late cornified envelope 3D (LCE3D), tumor necrosis factor ligand superfamily member 10 (TNFSF10), and CD247 were determined as key comorbidity genes, enriched in the proteasome and olfactory conduction pathways.

AURKB, CXCL11, LCE3D, TNFSF10, and CD247 were indicated as comorbid genes for PSO and CAD, and they therefore might be involved in the progression of these diseases.

Quercetin, a widely distributed flavonoid in medicinal plants, exhibits potent anti-cancer effects across various malignancies. However, its pharmacological activity in gastric cancer remains insufficiently characterized. To investigate the anti-proliferative, pro-apoptotic, anti-migration, and anti-tumor effects of Quercetin against gastric cancer using in vitro (human gastric adenocarcinoma cell line [AGS], human gastric carcinoma cell line [MKN-45]) and in vivo xenograft models.

Cell viability, apoptosis, migration, and invasion assays were performed following Quercetin treatment (0–200 µM). A nude mouse xenograft model was induced by subcutaneous inoculation of MKN-45 cells, followed by oral Quercetin treatment (50 or 100 mg/kg/day). Tumor growth, inflammatory cytokines, and oxidative stress biomarkers were evaluated.

Quercetin reduced the viability of AGS and MKN-45 cells in a dose-dependent manner, with IC₅₀ values of 46.3 and 52.7 µM, respectively. Apoptosis significantly increased under Quercetin treatment, while migration and invasion were markedly inhibited. In vivo, Quercetin suppressed tumor growth by up to 57.3% compared with controls and significantly reduced serum tumor necrosis factor-alpha, interleukin-6, interleukin-1β, and improved oxidative stress biomarkers.

Quercetin exerts strong therapeutic potential against gastric cancer by inhibiting proliferation, migration, and tumor progression, supporting its development as a natural product-based anti-cancer candidate.

Diabetic foot ulcer, a severe complication occurring in diabetic patients, lacks effective remedies at present.

The objective of this research is to investigate the impacts of exogenous irisin on diabetic wounds in mice and explore the associated mechanisms.

An animal model was constructed by administration of streptozotocin (STZ) (50 mg/kg) in mice to simulate a diabetic condition. A full-thickness excisional wound was produced on the dorsal skin of the mice to create a wound for the observation of the wound healing process. Cutaneous administration of 0.1 mL of exogenous irisin solution (1 µg/mL and 3 µg/mL) was applied to the injured tissue to assess the impact of exogenous irisin on the wound. Hematoxylin and eosin (H&E) staining assay was applied to evaluate histological changes in the skin tissue. The expression levels of endogenous irisin, adenosine 5′-monophosphate-activated protein kinase (AMPK), nuclear factor kappa B (NF-κB), and inflammatory factors in the skin tissue of the mice were measured by enzyme-linked immunosorbent assay (ELISA).

The results showed that irisin levels are positively correlated with the progress of wound healing. The STZ mice exhibited decreased pAMPK, increased NF-κB, and increased inflammatory cytokines. Exogenous irisin treatment restored these abnormal expressions in STZ mice. However, co-treatment with the AMPK inhibitor, Compound C, abolished exogenous irisin’s function of promoting wound healing and relieving inflammation.

Taken together, exogenous irisin possesses a therapeutic effect on skin wounds in STZ-induced diabetic mice, which is related to the regulation of inflammatory factors mediated by the AMPK–NF-κB pathway.

Sepsis-associated acute lung injury (SALI) is characterized by an uncontrolled inflammatory response and cell apoptosis, with macrophage apoptosis playing a key role in alveolar barrier disruption. Spermidine (SP), as a natural polyamine, has shown potential in anti-aging and immune regulation, but its intervention effect and mechanism on macrophage apoptosis in SALI are not yet clear.

This study aimed to investigate the interventional effect of SP on macrophage apoptosis in SALI and to elucidate its potential molecular mechanism.

A mouse SALI model was constructed by cecal ligation, and the intervention was performed by intraperitoneal administration of SP. Observe the phenotype of lung injury in SALI mice and the release of pro-inflammatory cytokines. Mechanistically, network pharmacology analysis was used to determine the potential mechanism of SP treatment for SALI and conduct experimental validation.

The results showed that SP treatment significantly reduced the wet-to-dry ratio of lung tissue and the amount of protein exudation in bronchoalveolar lavage fluid, inhibiting the release of pro-inflammatory factors interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and alleviating alveolar structural damage. Mechanistically, we employed network pharmacology analysis to indicate that the key mechanism of SP’s therapeutic effect on SALI lies in its anti-apoptotic properties. Immunoblot analysis further showed that SP treatment reduced the expression of pro-apoptotic proteins cleaved-caspase 9/3, and Bax in lung tissue, while upregulating the anti-apoptotic protein Bcl-2.

This study elucidates for the first time the mechanism by which SP alleviates SALI by targeting the macrophage apoptosis pathway, providing experimental evidence for the development of lung protection strategies based on immune metabolism regulation.

Lung cancer is a foremost global health challenge and remains the leading cause of cancer-related mortality worldwide. Despite advancements in early diagnosis and treatment, most cases are detected at advanced stages, which severely compromises survival rates. Current chemotherapeutic agents are often limited by toxicity and resistance, highlighting the urgent need for safer and more effective preventive strategies.

The present study evaluated the chemopreventive potential of ajmalicine, an indole alkaloid, against benzo(a)pyrene (B(a)P)-induced lung carcinogenesis in rats.

Lung carcinogenesis was induced by oral administration of B(a)P for 4 consecutive weeks. Ajmalicine (20 mg/kg) was administered orally 1 week before and throughout the 16-week experimental period. Post-treatment, antioxidant status, xenobiotic detoxification enzymes, inflammatory cytokines, and caspase-3/9 activities were measured using standard commercial kits. Histopathological examination of lung tissues was performed to confirm the protective role of ajmalicine.

Ajmalicine treatment significantly enhanced antioxidant markers while reducing xenobiotic detoxification enzyme activity in B(a)P-exposed rats. Furthermore, ajmalicine attenuated pro-inflammatory cytokines and increased caspase-3/9 activity, suggesting the induction of apoptosis. Histopathological findings corroborated its protective role by demonstrating improved lung tissue architecture.

These findings reveal, for the first time, that ajmalicine exhibits strong chemopreventive effects against B(a)P-induced lung carcinogenesis by modulating oxidative stress, inflammation, and apoptosis. Ajmalicine may represent a promising natural candidate for preventing carcinogen-induced lung cancer.

Cataracts remain the foremost cause of preventable blindness globally, with oxidative stress serving as a central contributor to their pathogenesis. Given the limited accessibility of surgical intervention in many populations, there is a pressing need for effective non-surgical therapeutic alternatives. We aimed to explore the protective role of piperitone against cataract development in experimental rodents.

We aimed to explore the protective role of piperitone against cataract development in experimental rodents.

In the present study, cataracts were experimentally triggered in rat pups via a solitary subcutaneous dose of sodium selenite on post-natal day 12. Piperitone was administered at two different doses to evaluate its potential in mitigating cataractogenesis. Antioxidant capacity, oxidative stress markers, and indicators of lens protein oxidation were quantified to determine the compound’s antioxidative efficacy. Additionally, lens ascorbic acid levels and total calcium content were measured to assess their impact on lens clarity. Inducible nitric oxide synthase, cyclooxygenase-2, and nuclear factor kappa B were measured to investigate piperitone’s anti-inflammatory action. Furthermore, key components of the nuclear factor erythroid 2-related factor 2 (Nrf2) redox signaling pathway were evaluated to elucidate the underlying antioxidant mechanism. Lens opacification scores were recorded as a direct measure of cataract progression.

The findings revealed that piperitone significantly enhanced antioxidant defenses, reduced oxidative damage and protein modification in the lens, and suppressed inflammatory signaling. It also modulated redox homeostasis via activation of the Nrf2 pathway and led to a marked reduction in lens opacity.

Collectively, our data support the therapeutic efficacy of piperitone as an antioxidant agent for the prevention or delay of cataract development.

Cataracts, characterized by the gradual opacification of the crystalline lens, represent a primary cause of vision impairment worldwide, placing a considerable burden on individuals and healthcare systems. Understanding the precise mechanisms behind cataract formation is essential to developing targeted preventive and treatment approaches.

The current study was performed to investigate the preventive mechanisms of tomatidine against selenite-induced cataractogenesis in a rat pup model.

Cataracts were experimentally induced in rat pups by administering sodium selenite, followed by administration of tomatidine at dosages of 10 and 20 mg/kg, respectively. The lens opacification level, oxidative stress biomarker levels, calcium, and ascorbic acid concentrations in the lens tissues of rat pups were assessed. The concentrations of antioxidants, inflammatory cytokines, nuclear factor erythroid 2-related factor 2 (Nrf-2), nuclear factor-κB (NF-κB), and cyclooxygenase-2 (COX-2) were evaluated in the lenses of rat pups using kits.

The results of this study indicate that tomatidine administration significantly diminished lens opacification level, calcium, oxidative stress biomarkers, and increased ascorbic acid and antioxidant levels in the lens tissues of cataract-induced rat pups. Moreover, the tomatidine treatment significantly reduced the inflammatory cytokine levels, elevated antioxidant concentrations, reduced COX-2 and NF-κB levels, and enhanced Nrf-2 levels in the lens tissues of cataract-induced rat pups.

The findings of this study suggested that tomatidine may be effective in preventing the formation of selenite-induced cataract in rat pups. These outcomes highlight that tomatidine shows promise as a potential therapeutic agent for cataracts.

Myocardial infarction (MI) continues to be a leading contributor to illness and death worldwide, even in the face of substantial therapeutic and preventive interventions. Polygala tenuifolia, a traditional medicinal herb rich in diverse bioactive compounds, exhibits a broad range of therapeutic effects; however, its cardioprotective role has not been fully elucidated.

The herein study was proposed to examine the cardioprotective efficacy of the ethanolic extract of P. tenuifolia (PTEE) and was assessed in an isoproterenol (ISO)-induced MI model using male Wistar albino rats.

Animals were randomly assigned to four groups: control, ISO-treated, and two groups pre- and co-treated with PTEE for 20 days, followed by ISO administration on days 19 and 20. On day 21, blood and heart tissue samples were collected for biochemical and molecular analyses.

PTEE administration modulated serum biochemical parameters, enhanced antioxidant defense, stabilized myocardial ionic balance, reduced pro-inflammatory cytokine levels, and regulated nuclear factor kappa B/heme oxygenase-1/NAD(P)H quinone oxidoreductase-1 (NF-κB/HO-1/NQO-1) signaling pathways in MI-induced rats. Overall, PTEE exhibited significant cardioprotective activity by mitigating oxidative and inflammatory damage.

The present results imply that PTEE may be pursued as a therapeutic option for managing MI and allied cardiovascular disorders; however, further mechanistic and long-term studies are warranted to substantiate its clinical applicability.

Breast cancer is the most common cancer type in women globally, constituting a substantial portion of all documented female malignancies. It is the second major cause of cancer-associated mortality in women, with over one million new diagnoses each year.

The present work evaluated the anti-cancer activity of amarogentin by assessing its growth-inhibition and apoptosis-triggering capabilities against breast cancer cells.

The cytotoxic effects of amarogentin at various dosages on MDA-MB-231 cells were evaluated using the MTT test. The incidences of apoptosis in amarogentin-induced cells were evaluated using a dual staining technique. The concentrations of oxidative stress markers and PI3K/AKT/mTOR proteins were evaluated in amarogentin-treated cells utilizing kits.

The current findings demonstrate that the MDA-MB-231 cell viability was diminished after treatment with diverse dosages of amarogentin. The amarogentin treatment significantly enhanced apoptotic incidences in MDA-MB-231 cells, as seen by the dual staining assay results. The amarogentin treatment elevated thiobarbituric acid reactive substances level and subsequently diminished antioxidants in the MDA-MB-231 cells. Furthermore, amarogentin suppressed PI3K/AKT/mTOR proteins in the breast cancer cells.

The current findings indicate that amarogentin treatment significantly reduces cell viability and promotes oxidative stress-dependent apoptosis in breast cancer cells. Therefore, it has the potential to serve as an anti-cancer candidate for breast cancer treatment.

Globally, post-menopausal osteoporosis poses a major health challenge, primarily affecting elderly women because of its connection to lowered bone mineral density and increased susceptibility to fractures. This skeletal disorder not only compromises the quality of life but also contributes to a substantial socio-economic and healthcare burden.

We examined the efficacy of bavachin, a plant-derived flavonoid estrogen mimic, in mitigating osteoporosis in ovariectomized Wistar rats.

Osteoporotic conditions were established through bilateral ovariectomy (OVX), followed by treatment with bavachin. An additional OVX group received alendronate, a standard anti-osteoporotic drug, to serve as a reference for comparative efficacy. Critical molecular markers reflecting bone metabolism, such as osteocalcin, C-terminal telopeptide of type I collagen, alkaline phosphatase, and acid phosphatase, were quantified. Bone microarchitecture was examined using micro-computed tomography, while biomechanical strength was evaluated through a three-point bending test. Serum calcium and phosphorus levels were measured to examine bavachin’s influence on mineral homeostasis. Oxidative stress and inflammatory responses were analyzed by determining antioxidant enzyme activity and pro-inflammatory cytokine concentrations. Furthermore, the expression of bone remodeling regulators, such as osteoprotegerin (OPG), receptor activator of nuclear factor κB ligand (RANKL), osterix (Osx), and runt-related transcription factor 2 (Runx2), was examined in treated and untreated OVX rats.

Bavachin treatment attenuated oxidative stress and inflammation, while improving bone turnover markers and mechanical properties. A decrease in RANKL expression and an upregulation of OPG, Osx, and Runx2 suggest that bavachin effectively modulates bone remodeling pathways and inhibits osteoclast-mediated bone resorption.

Our findings demonstrate that bavachin exhibits significant anti-osteoporotic activity and may serve as a promising and safer alternative to conventional osteoporosis therapies.