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Background Rheumatoid arthritis (RA) is associated with joint damage. Effectiveness of embelin has been established in a wide variety of inflammatory disorders, but its utility as a therapeutic agent is limited by its poor absorption, rapid metabolism, and fast systemic elimination. To apprehend these limitations, we propose to use highly bioavailable embelin‐loaded chitosan nanoparticles (CS‐embelin NPs) for the treatment of RA. Methods The rats were made arthritic using a subcutaneous injection with 0.1 ml complete Freund's adjuvant (CFA) into the footpad of the left hind paw. CS‐embelin NPs (25 and 50 mg/kg) was administered from day 15 to day 28 after adjuvant injection. After the experimental period, the animals were sacrificed and various biochemical markers were assessed. Results Arthritic score and paw swelling were significantly reduced after treatment with CS‐embelin NPs. Arthritis‐induced rats showed a significant increase in malondialdehyde (MDA) and nitric oxide (NO) with a concomitant reduction of antioxidants in the paw tissue. CS‐embelin NPs (25 and 50 mg/kg) reduced MDA and NO levels and restored antioxidant levels to normalcy by mitigating oxidative stress. The arthritic rats exhibited elevated tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6) and interleukin‐1beta (IL‐1β) serum concentrations, upregulated TNF‐ α and IL–6 protein levels and upregulated nuclear factor‐kB (NF‐kB) mRNA expression in paw tissues. Treatment with CS‐embelin NPs (25 and 50 mg/kg) significantly reduced serum levels and down‐regulated inflammatory markers to normalcy, dose‐dependently. Conclusion The results suggest that CS‐embelin NPs displayed a protective effect against adjuvant‐induced arthritis in rats mediated through antioxidant and anti‐inflammatory effects.

Dipeptidyl peptidase-4 inhibitor (DPP-4 inhibitor) such as sitagliptin has been presented as antidiabetic drugs and has numerous restorative advantages over different diseases; however, its defensive role against aflatoxin b1 (AFB1) liver toxicity has not been previously examined. Wistar rats (65 weeks, male) were utilized in the investigation. Animals were divided into five different groups (n = 10): control; AFB1; AFB1 + Sita (50); AFB1 + Sita (100); and Sita (100). Sitagliptin significantly (*p ≤ .05, **p ≤ .01, and ***p ≤ .001) altered the levels of various serum liver enzymes (lactate dehydrogenase, alkaline phosphate, aspartate aminotransferase, and alanine aminotransferase). It decreased the concentration of an oxidative stress marker, that is, malondialdehyde and increased the level of antioxidant enzymes such as reduced glutathione, catalase, superoxide dismutase, and glutathione peroxidase in AFB1-administered rats. It also improved the Nrf2 expression and HO-1 level in AFB1-intoxicated rats. This investigation discusses innovative evidence on the protective role of sitagliptin against AFB1-induced hepatotoxicity in rats.

Homocysteine [HSCH2CH2CH(NH2)COOH] (Hcy) is a sulfur‐containing amino acid of 135.18 Da of molecular weight, generated during conversion of methionine to cysteine. If there is a higher accumulation of Hcy in the blood, that is usually above 15 µmol/L, it leads to a condition referred to as hyperhomocysteinemia. A meta‐analysis of observational study suggested an elevated concentration of Hcy in blood, which is termed as the risk factors leading to ischemic heart disease and stroke. Further experimental studies stated that Hcy can lead to an increase in the proliferation of vascular smooth muscle cells and functional impairment of endothelial cells. The analyses confirmed some of the predictors for Hcy presence, such as serum uric acid (UA), systolic blood pressure, and hematocrit. However, angiotensin‐converting enzyme inhibitors angiotensin‐converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) alone are inadequate for controlling UA and creatinine level, although the addition of folic acid may be beneficial in hypertensive patients who are known to have a high prevalence of elevated Hcy. We hypothesized that combination therapy with an ARB (olmesartan) and folic acid is a promising treatment for lowering the UA and creatinine level in hyperhomocysteinemia‐associated hypertension.

Rheumatoid arthritis (RA) is a chronic and accelerated autoimmune illness with proliferative and damaging synovitis, resulting in joint death and cartilage and bone erosion. This study focused on the potential therapeutic effect of wogonin on complete Freund's adjuvant (CFA) induced RA in rats and the underlying mechanisms. Arthritis was experimentally caused in rats by subcutaneously injecting 0.1 mL of CFA into the subplantar area of the left hind paw under moderate anesthesia on day zero. The regular oral doses of indomethacin/wogonin began on day zero and proceeded after injection to day 35. Wogonin reduced arthritic score considerably, enhanced body weight, and reduced paw thickness. Wogonin also boosted red blood cell considerably along with hemoglobin and reduced white blood cell count and erythrocyte sedimentation rate. Wogonin substantially improved an altered level of oxidative stress markers, antioxidant proteins, and inflammatory cytokines in a dose‐dependent way. Wogonin inhibited p38 phosphorylation triggered by CFA and p65 nuclear translocation.