Background: Methotrexate (MTX) is a folic acid antagonist, commonly administered for the treatment of a variety of cancers. However, methotrexate toxicity including bone marrow suppression and hepatic and renal toxicity limits its use. Angiotensin AT₁ receptor blockers including Valsartan (Val) possess the ability to ameliorate MTX-induced toxicity through various mechanisms. In this study, we explored the potential reno-protective effects of Val against MTX-induced acute kidney injury in rats. Methods: Twenty-four Wistar rats were randomly segregated into 3 groups. Group 1 served as the control group and received an oral dose of 1mL/kg of normal saline. Group 2 received a single dose of 20 mg/kg of MTX intraperitoneally (IP) for 5 days. Group 3 received a single IP dose of 20 mg/kg of MTX followed by an oral dose of 10 mg/kg of Valsartan for 5 days. At the end of the experiment, the levels of serum kidney biomarkers, inflammatory and oxidative stress markers were accessed. Furthermore, the effect of MTX on kidney tissue histology was examined. Results and discussion: Our results showed that MTX treatment increased the level of serum kidney and inflammatory biomarkers and decreased the level of antioxidants SOD and GSH while increasing the lipid peroxidation contents. Furthermore, MTX treatment caused structural changes to kidney histology. However, the administration of Val significantly prevented these changes. Conclusion: Valsartan possesses nephroprotective potential and might serve as a potential therapeutic strategy against MTX-induced kidney injury.

The present study explores the simple and eco-friendly green synthesis of silver (AgNPs) and gold (AuNPs) nanoparticles using aqueous flower extract of Bombax ceiba, commonly known as silk cotton. The extract, rich in flavonoids, serves as both a reducing and capping agent, facilitating the synthesis of metal nanoparticles. The synthesized nanoparticles were characterized using UV spectroscopy and scanning electron microscopy (SEM), confirming their formation and stability. The antibacterial activity of the AgNPs, AuNPs, and crude flavonoids was evaluated against several bacterial strains, including Salmonella typhi, Escherichia coli, Pseudomonas aeruginosa, Bacillus subtilis, and Staphylococcus aureus, using the agar well diffusion method. Our results show that AgNPs exhibit significant antibacterial activity, particularly against Gram-negative bacteria, with a marked zone of inhibition observed for S. typhi and E. coli. The inhibition zone increased with higher concentrations of AgNPs. In contrast, AuNPs and flavonoid solutions demonstrated only mild antibacterial effects, with no significant inhibition observed at lower concentrations (1–6 µL). The antibacterial efficacy of AgNPs was comparable to that of standard antibiotics, such as Azithromycin for Gram-positive bacteria and Ciprofloxacin for Gram-negative bacteria, suggesting their potential as effective antimicrobial agents. The antibacterial activity of the synthesized nanoparticles and the crude flavonoid extract highlights the promising use of Bombax ceiba flower extract in the green synthesis of metal nanoparticles with potential biomedical applications.

Introduction: Amiodarone (AMIO) is one of the most prescribed antiarrhythmic medications and is commonly used to treat atrial and ventricular fibrillations. A notable adverse effect of AMIO is pulmonary fibrosis. Cannabinoid (O-2545) has been shown to exert antioxidant, anti-inflammatory, and antifibrotic effects in both in vivo and in vitro experimental models. The present study aimed to investigate whether cannabinoid (O-2545) may attenuate amiodarone-induced pulmonary fibrosis in male Wistar rats. Methods: A regimen of 50 mg/kg AMIO was administered via oral gavage daily for 10 consecutive days to induce acute pulmonary fibrosis. The experiment included 24 Wistar rats assigned to four groups. The control group received daily subcutaneous injections of normal saline for the same time period. The AMIO group received a daily oral gavage of AMIO (50 mg/kg) for 10 days. Concurrently, the O-2545 group received daily oral doses of cannabinoid. The combined treatment group received both AMIO and cannabinoid orally each day for 10 days. Results: High-dose AMIO (50 mg/kg) administration resulted in a significant elevation of oxidative stress, followed by a decrease in antioxidant function, an increase in inflammatory cytokines, fibrosis markers, and apoptosis. Pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and adenosine (Adens), apoptotic markers tumor protein p53 (p53) and caspase 3 protein (caspase-3), oxidative stress malondialdehyde (MDA), fibrosis indicator hydroxyproline (HYDROX), and histone deacetylase (HDAC) activity, accompanied by a marked reduction in the antioxidant glutathione (GSH), compared to the control group. Histopathological examination of pulmonary tissues revealed that O-2545 significantly mitigated AMIO-induced pulmonary fibrosis. In conclusion, the results showed that cannabinoid (O-2545) may offer significant therapeutic potential in mitigating pulmonary toxicity induced by AMIO in rats. Purpose: This study investigates the possible protective therapeutic effects of (O-2545) on AMIO-induced pulmonary fibrosis in Wistar rats.

Background: A member of the quinoxaline family, 2,3-dimethylquinoxaline (DMQ), has been evaluated for associated nephroprotective properties in an in vivo model system to assess renal inflammation induced by the anticancer drug doxorubicin (DOX). Methods: Rats were administered DMQ at doses of 30 or 60 mg/kg body weight once daily for 7 consecutive days. Additionally, a single intraperitoneal (i.p.) dose of DOX (15 mg/kg body weight) was administered on the sixth day. DMQ-mediated nephroprotective effects were assessed by measuring renal function markers, oxidative stress markers, lipid peroxidation, renal stress markers, proinflammatory cytokines, and inflammatory mediator levels, as well as by performing histopathological examination of kidney tissues. Results: DMQ-treated rats exhibited a marked reduction in kidney toxicity markers and restoration of antioxidant enzyme levels, leading to attenuated oxidative stress. DMQ administration also reduced proinflammatory cytokines, renal stress markers, and inflammatory mediators. Furthermore, DMQ may also attenuate DOX-induced renal structural damage and help restore the dilated capsular space and other histopathological alterations in kidney tissues. Conclusion: These findings suggest that DMQ may protect against DOX-induced renal damage by alleviating oxidative stress and inflammation in a rat model, indicating the potential of DMQ as a nephroprotective agent.