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Patulin (PAT) is a mycotoxin frequently detected in moldy fruits and fruit products. This study investigated the protective role of glutathione (GSH), an antioxidant agent, against PAT-induced cytotoxicity and its potential mechanisms in HEK293 cells. The obtained results showed that the addition of GSH significantly increased cell viability and decreased apoptosis induced by PAT. Additionally, GSH decreased intracellular ROS and mitochondrial ROS overproduction, suppressed the decline of the mitochondrial membrane potential, and maintained cellular ATP contents. GSH prevented the impairment of mitochondrial oxidative-phosphorylation system and, especially, enhanced the mRNA and protein levels of electron-transport-chain complex III (UQCRC2) and complex V (ATP5, ATP6 and ATP8). Furthermore, GSH increased endogenous GSH contents; enhanced the antioxidant-enzyme activities of SOD, CAT, GR, and GPx; and modulated oxidative damage. These results suggest that GSH reduces PAT-induced cytotoxicity via inhibition of oxidative damage and the mitochondrial apoptotic pathway in HEK293 cells.

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Aristolochic acid I (AA-I) remains a leading cause of aristolochic acid nephropathy (AAN), however few prevention and treatment strategies exist. In this work, the nephroprotective effect of diosgenin, a steroidal...

Linarin is a natural flavonoid compound found in Chrysanthemum indicum, Mentha species and other plants with various biological activities. The study aimed to investigate the protective effect of linarin supplementation...

Scope Diosgenin (DIO) is a natural steroid sapogenin presented in various plants. It exerts anti‐oxidant, anti‐inflammatory and anti‐diabetic nephropathy properties. The present study evaluates the intervention effect of DIO on nephrotoxicity induced by food contaminant 3‐chloro‐1, 2‐propanediol (3‐MCPD) in vivo and in vitro. Methods and Results Treatment with DIO (15 mg kg−1 d−1) in Sprague‐Dawley rats for 4‐week relieves kidney injury induced by 3‐MCPD (30 mg kg−1 d−1). In vitro, DIO (2, 6, and 8 µM) alleviates cell injury and apoptosis effectively in human embryonic kidney (HEK293) cells. DIO realizes its protective function via the regulation of endoplasmic reticulum (ER) stress and mitochondrial apoptosis pathway. Blockage of ER stress by 4‐phenylbutyric acid (4‐PBA), a specific ER stress antagonist, inhibits mitochondrial apoptosis, suggesting a connection between mitochondrial apoptosis and ER stress. Furthermore, the study demonstrates that the maintenance of Ca2+ homeostasis and Bcl2 expression, two main targets of ER stress, contributes to the protection role of DIO on mitochondrial‐dependent apoptosis. In addition, DIO relieves the impairment of oxidative phosphorylation. Conclusion This study demonstrates that DIO exerts protective effect against kidney injury, mitochondrial dysfunction, and apoptosis through the inhibition of ER stress and the further maintenance of Ca2+ homeostasis and Bcl2 expression.

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