Protective effects of protocatechuic acid against cisplatin-induced renal damage in rats

• Oxidative renal cell damages were inhibited by protocatechuic acid co-treatment.
• Renal dysfunction was attenuated by protocatechuic acid administration in rats.
• Elevated pro-caspase-3 levels of rat kidneys were reduced by protocatechuic acid.
• Protocatechuic acid alleviates cisplatin-induced oxidative renal damage.

The protective effects of an extract from bitter melon (Momordica charantia, Cucurbitaceae) against oxidative stress was previously reported and found that protocatechuic acid (PCA) was one of the major phenolic constituents in the extract. The renoprotective effect of PCA from bitter melon was investigated in the present study. In the LLC-PK1 cellular model, the decline in cells viabilities induced by oxidative stress, such as that induced by sodium nitroprusside, pyrogallol, and SIN-1, was significantly and dose-dependently inhibited by PCA. In the in vivo model, the cisplatin-treated rats showed increased plasma levels of creatinine, decreased creatinine clearance, and increased urine protein levels. However, these parameters related to renal dysfunction were markedly attenuated by PCA treatment. Administration of PCA resulted in remarkable improvement in the histological appearance and reduction in tubular cell damage in the cisplatin-treated rat kidneys. Moreover, the elevated levels of pro-caspase-3 induced by cisplatin in rat kidneys were down-regulated by PCA co-treatment. These results suggest that PCA has protective activity against anticancer drug-induced oxidative nephrotoxicity.

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