Key result
Combined treatment with baicalein and alpha-tocopherol effectively prevented cisplatin-induced nephrotoxicity by augmenting antioxidant status and reducing inflammatory markers.
Why the study?
Cisplatin causes serious toxicity linked to oxidative stress and inflammation, prompting exploration into the protective effects of baicalein and alpha-tocopherol against cisplatin-induced nephrotoxicity.
Does baicalein and alpha-tocopherol prevent cisplatin-induced nephrotoxicity in rats?
Does baicalein and alpha-tocopherol prevent cisplatin-induced nephrotoxicity in rats?
The combination of baicalein and alpha-tocopherol attenuates cisplatin-induced nephrotoxicity in rats by modulating oxidative stress and inflammatory pathways.
Hypothesis-generating in rats; clinical trials needed before considering baicalein plus alpha-tocopherol for cisplatin nephroprotection.
Cisplatin (CP) is a conventional chemotherapeutic agent with serious adverse effects. Its toxicity was linked to the stimulation of oxidative stress and inflammation. As a result, this study explored the protective effect of baicalein and alpha-tocopherol in nephrotoxicity induced by cisplatin. Until receiving an intraperitoneal injection of CP (3 mg/kg BW), rats were given baicalein orally 100 mg/kg for seven days or/and a single intraperitoneal injection of α-tocopherol 250 mg/kg. Renal function was tested to explore whether baicalein and α-tocopherol have any beneficial effects; blood urea nitrogen (BUN), serum creatinine, malondialdehyde (MDA) content, antioxidant activity biomarkers and histopathology of renal tissue, oxidative stress biomarkers, inflammatory response markers, and histopathological features of kidney architecture were measured. Cisplatin treatment resulted in extreme renal failure, as measured by high serum creatinine and BUN levels and severe renal changes. Cisplatin therapy resulted in increased lipid peroxidation and decreased glutathione and superoxide dismutase levels, reflecting oxidative stress. Upon treatment with α-tocopherol, baicalein, and combined therapy, there was augmentation in the antioxidant status as well as a reduction in IL-6, NF-κB, TNF, TLR2, and TLR4 and a significant increase in Keap-1 and NRF-2. The combined treatment was the most effective and the nearest to the normal status. These findings suggest that baicalein and α-tocopherol may be useful in preventing cisplatin-induced nephrotoxicity.
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Awadalla et al. (2022) studied Cisplatin-induced nephrotoxicity. Baicalein and alpha-tocopherol vs. Cisplatin alone was evaluated on Renal function, oxidative stress biomarkers, inflammatory response markers, and histopathology. Combined treatment with baicalein and alpha-tocopherol effectively prevented cisplatin-induced nephrotoxicity by augmenting antioxidant status and reducing inflammatory markers.
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