ArticleJournal of molecular histology2025
Renoprotective effect of polyphenolic-rich extract of Phyllanthus niruri in streptozotocin-induced diabetic nephropathy via moderation of oxidative stress and inhibition of kidney injury.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Studies have underlined the relevance of plants as sources of medicament for diabetes mellitus its sequelae. This research sought to appraise the renal-protective effect of the polyphenolic-rich extract of Phylanthus niruri (PEPN) leaves in Wistar rats made diabetic with streptozotocin. Fifty-six rats were arbitrarily grouped into seven places (n = 8). Standard procedure was used to extract polyphenols from the leaves using 80% acetone. Experimental groups included normal control, diabetic untreated, as well as diabetic groups managed with 5/500 mg/kg bw glibenclamide/metformin and diabetic groups each treated with 50, 75, 100 and 125 mg/kg bw PEPN. The study lasted for 28 days. After treatment period, standard procedures were used to evaluate activities of antioxidant enzymes and kidney injury markers in the kidney, while levels of creatinine, urea and uric acid were measured in the serum. Findings show that treatment of diabetic rats with PEPN led to a significant (p < 0.05) lowering of serum uric acid, urea and creatinine when compared with diabetic control group. Similarly, the administration of PEPN led to a significant (p < 0.05) elevation of enzymatic functions of superoxide dismutase and catalase in the kidney, with a concomitant reduction in malondialdehyde. In addition, PEPN therapy in diabetic rats with PEPN significantly (p < 0.05) diminished mRNA levels of kidney injury marker 1 and neutrophil gelatinase-associated lipocalin in the kidney when compared to untreated diabetic rats. Therefore, it could be concluded that PEPN could confer renoprotection in diabetic rats by enhancing the antioxidant system and suppression of kidney injury marker genes.
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