Tinnitus is the perception of phantom noise without any external auditory sources. The degeneration of the function or activity of the peripheral or central auditory nervous systems is one of the causes of tinnitus. This damage has numerous causes, such as loud noise, aging, and cytotoxicity. All these sources excite the cells of the auditory pathway, producing reactive oxygen species that leads to the death of sensory neural hair cells. This causes involuntary movement of the tectorial membrane, resulting in the buzzing noise characteristic of tinnitus. Autophagy is an evolutionarily conserved catabolic scavenging activity inside a cell that has evolved as a cell survival mechanism. Numerous studies have demonstrated the effect of autophagy against oxidative stress, which is one of the reasons for cell excitation. This review compiles several studies that highlight the role of autophagy in protecting sensory neural hair cells against oxidative stress-induced damage. This could facilitate the development of strategies to treat tinnitus by activating autophagy.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro. METHODS: CQ (10 or 30 mg/kg/day; i.p.) was injected for three weeks, and fasting blood glucose levels, glucose tolerance, and liver lipid metabolism were assessed. RESULTS: CQ administration alleviated the increase in body and liver weights and improved glucose tolerance in NAFLD mice model. CQ also reduced the gene expression levels of lipid biosynthesis and inflammation markers, while increasing the levels of fatty acid oxidation markers in liver tissues and HepG2 cells. These beneficial effects of CQ were mediated via activation of the sirtuin 1 (SIRT1)/adenosine monophosphate-activated protein kinase (AMPK) signalling pathway in vitro and in vivo. CONCLUSION Collectively, our data suggest that CQ improves liver lipid metabolism and reduces blood glucose levels via activation of the SIRT1/serine/threonine kinase 11 (STK11/LKB1)/AMPK axis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro. METHODS: CQ (10 or 30 mg/kg/day; i.p.) was injected for three weeks, and fasting blood glucose levels, glucose tolerance, and liver lipid metabolism were assessed. RESULTS: CQ administration alleviated the increase in body and liver weights and improved glucose tolerance in NAFLD mice model. CQ also reduced the gene expression levels of lipid biosynthesis and inflammation markers, while increasing the levels of fatty acid oxidation markers in liver tissues and HepG2 cells. These beneficial effects of CQ were mediated via activation of the sirtuin 1 (SIRT1)/adenosine monophosphate-activated protein kinase (AMPK) signalling pathway in vitro and in vivo. CONCLUSION Collectively, our data suggest that CQ improves liver lipid metabolism and reduces blood glucose levels via activation of the SIRT1/serine/threonine kinase 11 (STK11/LKB1)/AMPK axis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro. METHODS: CQ (10 or 30 mg/kg/day; i.p.) was injected for three weeks, and fasting blood glucose levels, glucose tolerance, and liver lipid metabolism were assessed. RESULTS: CQ administration alleviated the increase in body and liver weights and improved glucose tolerance in NAFLD mice model. CQ also reduced the gene expression levels of lipid biosynthesis and inflammation markers, while increasing the levels of fatty acid oxidation markers in liver tissues and HepG2 cells. These beneficial effects of CQ were mediated via activation of the sirtuin 1 (SIRT1)/adenosine monophosphate-activated protein kinase (AMPK) signalling pathway in vitro and in vivo. CONCLUSION Collectively, our data suggest that CQ improves liver lipid metabolism and reduces blood glucose levels via activation of the SIRT1/serine/threonine kinase 11 (STK11/LKB1)/AMPK axis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro. METHODS: CQ (10 or 30 mg/kg/day; i.p.) was injected for three weeks, and fasting blood glucose levels, glucose tolerance, and liver lipid metabolism were assessed. RESULTS: CQ administration alleviated the increase in body and liver weights and improved glucose tolerance in NAFLD mice model. CQ also reduced the gene expression levels of lipid biosynthesis and inflammation markers, while increasing the levels of fatty acid oxidation markers in liver tissues and HepG2 cells. These beneficial effects of CQ were mediated via activation of the sirtuin 1 (SIRT1)/adenosine monophosphate-activated protein kinase (AMPK) signalling pathway in vitro and in vivo. CONCLUSION Collectively, our data suggest that CQ improves liver lipid metabolism and reduces blood glucose levels via activation of the SIRT1/serine/threonine kinase 11 (STK11/LKB1)/AMPK axis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition that increase the risk of simple steatosis to hepatocellular carcinoma. This study aimed to investigate the biological effects of camphorquinone (CQ) in a high-fat diet (HFD)-fed and low dose streptozotocin (STZ)-induced mouse model, widely used to mimic the concurrent development of NAFLD pathological conditions in vivo, and a free fatty acid-induced hepatic steatosis cell model in vitro. METHODS: CQ (10 or 30 mg/kg/day; i.p.) was injected for three weeks, and fasting blood glucose levels, glucose tolerance, and liver lipid metabolism were assessed. RESULTS: CQ administration alleviated the increase in body and liver weights and improved glucose tolerance in NAFLD mice model. CQ also reduced the gene expression levels of lipid biosynthesis and inflammation markers, while increasing the levels of fatty acid oxidation markers in liver tissues and HepG2 cells. These beneficial effects of CQ were mediated via activation of the sirtuin 1 (SIRT1)/adenosine monophosphate-activated protein kinase (AMPK) signalling pathway in vitro and in vivo. CONCLUSION Collectively, our data suggest that CQ improves liver lipid metabolism and reduces blood glucose levels via activation of the SIRT1/serine/threonine kinase 11 (STK11/LKB1)/AMPK axis.