Current pharmaceutical biotechnology · 2026
Protective Role of Coffee in Thioacetamide-induced Nephrotoxicity: A Study in Rats.
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Zaidi Syeda Nuzhat Fatima, Mohiuddin Amna, Gojayev Anar, Jan Afnan, Muhsinah Abdullatif Bin, Khan Ajmal
Аннотация
OBJECTIVES: The purpose of the present research was to assess the protective role of coffee in thioacetamide-induced nephrotoxicity.
METHODS: The experimental period consisted of 18 weeks, divided into two phases. Four experimental groups were designed, each consisting of six rats. Group I was considered an untreated control group. Groups II and III were intraperitoneally injected with thioacetamide at a dose of 200 mg/kg body weight twice a week for twelve weeks during the first phase of the study. In the second phase, group II received saline, and group III and group IV received 0.4 mg/Kg of coffee daily for six weeks. The biochemical analysis was evaluated by the estimation of plasma urea, uric acid, creatinine, Malondialdehyde (MDA), Superoxide Dismutase (SOD), and catalase.
RESULTS: Thiocetamide-induced nephrotoxicity resulted in the reduction of body weight, superoxide dismutase, and catalase activities, and an increase in kidney weight, plasma urea, uric acid, creatinine, and tissue malondialdehyde. Supplementation with coffee effectively increased body weight while reducing elevated levels of urea, uric acid, creatinine, and MDA. It also restored SOD and catalase activities in Group III (TAA + Coffee-treated).
CONCLUSION: This work shows that coffee can protect the kidneys against thioacetamide-induced nephrotoxicity in a rat model. It highlights the antioxidant potential of coffee by its ability to restore enzymatic antioxidant activity (SOD and catalase), lower oxidative stress markers (MDA), and enhance renal function measures (urea, creatinine, and uric acid). The study fills a significant gap by demonstrating coffee as a viable natural therapeutic agent for oxidative stressinduced kidney impairment, providing an alternative to conventional treatments with fewer side effects.
METHODS: The experimental period consisted of 18 weeks, divided into two phases. Four experimental groups were designed, each consisting of six rats. Group I was considered an untreated control group. Groups II and III were intraperitoneally injected with thioacetamide at a dose of 200 mg/kg body weight twice a week for twelve weeks during the first phase of the study. In the second phase, group II received saline, and group III and group IV received 0.4 mg/Kg of coffee daily for six weeks. The biochemical analysis was evaluated by the estimation of plasma urea, uric acid, creatinine, Malondialdehyde (MDA), Superoxide Dismutase (SOD), and catalase.
RESULTS: Thiocetamide-induced nephrotoxicity resulted in the reduction of body weight, superoxide dismutase, and catalase activities, and an increase in kidney weight, plasma urea, uric acid, creatinine, and tissue malondialdehyde. Supplementation with coffee effectively increased body weight while reducing elevated levels of urea, uric acid, creatinine, and MDA. It also restored SOD and catalase activities in Group III (TAA + Coffee-treated).
CONCLUSION: This work shows that coffee can protect the kidneys against thioacetamide-induced nephrotoxicity in a rat model. It highlights the antioxidant potential of coffee by its ability to restore enzymatic antioxidant activity (SOD and catalase), lower oxidative stress markers (MDA), and enhance renal function measures (urea, creatinine, and uric acid). The study fills a significant gap by demonstrating coffee as a viable natural therapeutic agent for oxidative stressinduced kidney impairment, providing an alternative to conventional treatments with fewer side effects.