PROTECTIVE ROLE OF 2’,6’- DIHYDROXYACETOPHENONE IN MITIGATING DIABETES- DRIVEN HEPATIC INJURY IN RATS

Hepatoprotective effects of cinnamic acid against carbon tetrachloride–induced liver injury in a mouse model

Immunomodulatory and Inflammation-suppressive Effects of Arundo donax L. in a Hepatic Injury Model

The conclusion from this study can be helpful in the usage of AD as an adjuvant therapy that minimizes toxic effects of chemotherapy and improves treatment outcomes.

Rutin Protects Against Nonylphenol-Induced Reproductive Injury in Rats Via Modulation of Steriogenic, Inflammatory and Apoptotic Pathways

Rutin serves as an effective protective agent against NPL-associated infertility and reproductive failure by modulating steroidogenic, inflammatory, and apoptotic pathways and establishes a foundation for using natural polyphenols to counteract the reproductive risks posed by environmental contaminants.

Potential Involvement of Redox and Inflammatory Signalling in the Antihyperglycemic and Antioxidant Effects of Harmaline in Male Mice With Type 2 Diabetes

ABSTRACT Introduction Type 2 diabetes mellitus (T2DM) is strongly associated with oxidative stress and inflammation. Harmaline (HAR), an alkaloid with antioxidant and anti‐inflammatory properties, has been suggested to possess antidiabetic potential. This study investigated the effects of HAR in experimental T2DM and its association with changes in the nuclear factor erythroid 2‐related factor 2 (Nrf2) and nuclear factor kappa‐B (NF‐κB) pathways. Methods In vitro experiments were performed using mouse pancreatic cells cultured under different glucose concentrations to evaluate insulin secretion and antioxidant status. For the in vivo study, T2DM was induced in mice by nicotinamide (120 mg/kg) and streptozotocin (65 mg/kg). Fasting blood glucose (FBG) was measured 1 week after induction. Forty‐eight adult male NMRI mice were randomly assigned to four groups: normal control (NC), diabetic control (DC), HAR‐treated (30 mg/kg), and metformin‐treated (150 mg/kg). Treatments were administered once daily for 10 days. Results HAR enhanced insulin secretion and antioxidant capacity while reducing lipid peroxidation in vitro. In diabetic mice, HAR significantly reduced FBG, improved the lipid profile, and restored pancreatic antioxidant status. These effects were accompanied by increased expression of miR‐200a, Nrf2, and NAD(P)H: quinone oxidoreductase 1 and reduced Keap1 expression. In addition, HAR increased miR‐125b expression and reduced the expression of NF‐κB, TNF‐α, IL‐1β, and IL‐6. Decreased changes in RAS‐related markers were also observed after HAR treatment. Conclusion HAR improved glycemic control and pancreatic antioxidant status and reduced inflammatory responses in experimental T2DM. These beneficial effects were associated with modulation of Nrf2, NF‐κB, and RAS‐related signalling pathways, suggesting their potential involvement in the observed protective effects. Further studies are needed to establish the underlying mechanisms and evaluate the long‐term efficacy and safety of HAR.

Investigation of the Antioxidant Signalling Mechanisms of Rosmarinus officinalis L. in an Aniline-induced Splenic Toxicity Rat Model

Background: Aniline is an industrial chemical whose reactive metabolites induce oxidative stress and structural damage in splenic tissue, making aniline-induced splenic toxicity in rats a well-established experimental model for evaluating protective interventions. Rosmarinus officinalis L. (rosemary) possesses potent antioxidant and anti-inflammatory phytochemicals that may mitigate chemically induced tissue injury. Aim: To investigate the antioxidant-mediated splenoprotective effects of Ethanolic Rosemary Extract (ERE) against aniline-induced splenic toxicity in male Wistar rats. Methods: Male Wistar rats (200-250 g) were randomly divided into five groups (n = 6) and treated for 30 days. Splenic toxicity was induced by oral administration of aniline hydrochloride (50 mg/kg/day). Protective treatment groups received ERE at doses of 100 or 200 mg/kg/day orally, while citric acid (100 mg/kg/day, p.o.) served as the reference standard. Physiological parameters, oxidative stress biomarkers, antioxidant enzyme activities (GSH and CAT), ATPase activity, serum biochemical indices, histopathological changes, and hemosiderin deposition were assessed. Statistical analysis was performed using one-way ANOVA, with p<0.05 considered statistically significant. Results: Aniline administration produced splenomegaly, excessive iron accumulation, elevated lipid peroxidation, impaired antioxidant defences, reduced ATPase activity, and pronounced histopathological alterations including fibrosis and disruption of normal splenic architecture. Treatment with ERE significantly ameliorated these toxic effects in a dose-dependent manner. Rosemary extract restored antioxidant enzyme levels, reduced lipid peroxidation and nitric oxide production, improved ATPase activity, decreased hemosiderin deposition, normalised haematological and biochemical parameters, and preserved splenic histoarchitecture. The higher dose (200 mg/kg) demonstrated the greatest protective efficacy. Conclusion: ERE effectively protects against aniline-induced splenic toxicity by attenuating oxidative stress, restoring antioxidant defences, reducing iron accumulation, and preserving tissue architecture, suggesting its potential as a natural splenoprotective agent. Major Findings: ERE significantly ameliorated oxidative stress, restored antioxidant enzyme activity, improved haematological indices, reduced splenic iron overload, and preserved splenic histoarchitecture, with the 200 mg/kg dose producing the greatest protective effect.

"Radiation-Synthesized Gallotannin Hydrogel Attenuates Trisenox-Induced Nephrotoxicity in Rats: miR-223/TXNIP Axis Modulation of Oxidative Stress and Inflammation".

Arsenic trioxide (ATO) is a potent therapeutic agent against acute promyelocytic leukemia; nevertheless, its clinical utility is severely restricted by dose-limiting nephrotoxicity. This study investigated the protective potential of a radiation-synthesized gallotannin hydrogel (GTH) against ATO-induced kidney injury in rats. Forty male Wistar rats were randomized into four experimental groups: Control, ATO (4 mg/kg, i.p., for 4 weeks), GTH (2 mg/kg, i.p.), and ATO + GTH. GTH treatment was initiated during the third week of ATO administration, with GTH being administrated one hour prior to ATO injection. Following the experimental period, animals were sacrificed, tissue histology was examined, and renal function was assessed by serum urea and creatinine levels. Oxidative stress was evaluated via MDA, SOD, GSH, and GPx markers. Additionally, miR-223 and TXNIP expression levels were quantified using qRT-PCR. Inflammatory mediators (NF-κB, NLRP3, Caspase-1, IL-1β, and IL-18), endoplasmic reticulum (ER) stress markers (PERK, eIF2α, and CHOP), and the apoptotic marker caspase-3 were analyzed by ELISA. Our results revealed that GTH noticeably ameliorated kidney dysfunction, as evidenced by reduced serum urea and creatinine levels. Furthermore, GTH attenuated oxidative stress by decreasing MDA levels and restoring antioxidant enzyme activities (SOD, GSH, and GPx). Histological analysis confirmed that GTH mitigated structural renal damage. Molecularly, GTH administration suppressed the ATO-induced upregulation of miR-223 and TXNIP. This downregulation correlated with a reduction in inflammatory mediators, attenuation of ER stress markers, and decreased apoptosis. These findings demonstrate that radiation-synthesized gallotannin hydrogel (GTH) exerts nephroprotective effects against ATO-induced nephrotoxicity. These benefits are driven by antioxidant, anti-inflammatory, and anti-apoptotic mechanisms mediated via modulation of the miR-223/TXNIP axis.