Modified rougan decoction attenuates hepatocyte apoptosis through ameliorating mitochondrial dysfunction by upregulated SIRT1/PGC-1α signaling pathway

The modified rougan decoction (MRGD) compound formula has been proven a certain ability to relieve lipopolysaccharide-enrofloxacin (LPS-ENR)-induced liver oxidant injury in chickens. Recent advances have shown that mitochondrial dysfunction affects the development of many diseases, leading to increased interest in exploring its effects. Using LPS-ENR-injured in vivo and in vitro to further evaluate the effects of MRGD on mitochondrial structure and function, and emphasized further investigation of its molecular mechanism. After LPS-ENR treatment, the levels of inflammation and apoptosis markers were increased, along with higher mitochondrial injury. Results showed that MRGD reduced inflammatory factors expression and inhibited the nuclear translocation of NF-κB P65, reducing the inflammatory response in vivo and in vitro. Additionally, MRGD pretreatment inhibited mitochondrial dysfunction, mitochondrial oxidative stress, and mitochondrial pathway apoptosis by maintaining mitochondrial structure and function. Moreover, treatment with the inhibitor EX527 showed that MRGD promoted mitochondrial biogenesis ability through the SIRT1/PGC-1α pathway and interfered with mitochondrial dynamics, and activate Nrf2. In summary, MRGD played a key role in promoting mitochondrial function and thus alleviating hepatocyte apoptosis in vivo and in vitro at least in part.