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Emodin-Induced Oxidative Inhibition of Mitochondrial Function Assists BiP/IRE1/CHOP Signaling-Mediated ER-Related Apoptosis. | LitMetric

AI Article Synopsis

  • Cassiae Semen is a popular herbal medicine that can cause liver injury if not used properly, mainly due to a compound called emodin, although the exact causes are not fully understood.
  • This study investigates how emodin leads to cell death (apoptosis) in liver cells, focusing on the roles of oxidative stress, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress.
  • Results show that emodin triggers a chain reaction involving increased reactive oxygen species (ROS), ER stress, and mitochondrial damage, suggesting that targeting these stress pathways could help treat liver injuries linked to emodin.

Article Abstract

Cassiae Semen is a widely used herbal medicine and a popular edible variety in many dietary or health beverage. Emerging evidence disclosed that improper administration of Cassiae Semen could induce obvious liver injury, which is possibly attributed to emodin, one of the bioactive anthraquinone compounds in Cassiae Semen, which caused hepatotoxicity, but the underlying mechanisms are not completely understood. Hence, the present study firstly explored the possible role of oxidative stress-mediated mitochondrial dysfunction and ER stress in emodin-cause apoptosis of L02 cells, aiming to elaborate possible toxic mechanisms involved in emodin-induced hepatotoxicity. Our results showed that emodin-induced ROS activated ER stress and the UPR via the BiP/IRE1/CHOP signaling pathway, followed by ER Ca release and cytoplasmic Ca overloading. At the same time, emodin-caused redox imbalance increased mtROS while decreased MMP and mitochondrial function, resulting in the leaks of mitochondrial-related proapoptotic factors. Interestingly, blocking Ca release from ER by 2-APB could inhibit emodin-induced apoptosis of L02, but the restored mitochondrial function did not reduce the apoptosis rates of emodin-treated cells. Besides, tunicamycin (TM) and doxorubicin (DOX) were used to activate ER stress and mitochondrial injury at a dosage where obvious apoptosis was not observed, respectively. We found that cotreatment with TM and DOX significantly induced apoptosis of L02 cells. Thus, all the results indicated that emodin-induced excessive ROS generation and redox imbalance promoted apoptosis, which was mainly associated with BiP/IRE1/CHOP signaling-mediated ER stress and would be enhanced by oxidative stress-mediated mitochondrial dysfunction. Altogether, this finding has implicated that redox imbalance-mediated ER stress could be an alternative target for the treatment of Cassiae Semen or other medicine-food homologous varieties containing emodin-induced liver injury.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8084644PMC
http://dx.doi.org/10.1155/2021/8865813DOI Listing

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