Apelin and its receptor apj have a variety of biological functions and are involved in appetite and energy regulation. However, the comparative studies of apelin/apj system in fish are still absent. In this study, the open reading frames of apelin and apja and apjb were obtained. Apelin and apj mRNAs were widely distributed in all tissues detected, with the highest level in the brain, followed by the spleen, kidney and foregut. The mRNA expression of apelin and apj s increased rapidly at mealtime and significantly decreased after 30 min of feeding. In addition, there were obvious circadian rhythms (higher at nighttime and lower at daytime) in the expression of apelin and apja and apjb . Furthermore, fasting elevated the mRNA levels of apelin and apj s in the hypothalamus, foregut and hepatopancreas. When the 8-day fasted fish were refed, apelin and apj s mRNA expression significantly decreased. However, there were differences in the response to fasting and refeeding between apja and apjb . The roles of apelin and its receptor apjs in fish are poorly understood. Herein, we employed molecular and physiological studies to characterize their structures, distribution and mRNA expression responses to periprandial changes and fasting–refeeding in Cyprinus carpio L. for the first time.
Zhaoqi Wang,Duomao Lin,Boqun Cui,Dongni Zhang,Jinjing Wu,Jun Ma
Excessive or uncontrolled mitophagy may result in a drastic shortage of healthy mitochondrial for ATP supply after reperfusion, leading to irreversible myocardial damage . Melatonin , a hormone produced by the pineal gland, has been proven to ameliorate myocardial ischemia-reperfusion (I/R) injury via regulating mitophagy. However, its underlying mechanism has not been fully elucidated. The present study focused on the role of mitophagy in the cardioprotective effects of melatonin by using the myocardial I/R rat model. The rats were pretreated with or without the apelin inhibitor ML221, the sirtuin 3 (SIRT3) inhibitor 3-TYP and then subjected to I/R injury, with melatonin administrated 10 min before reperfusion. The effects of melatonin on myocardial infarct size, biomarkers of myocardial injury, oxidative stress , and mitochondrial function were detected, and the expression of apelin, SIRT3, and mitophagy-related proteins were also measured. Excessive mitophagy was activated after I/R injury and was correlated with oxidative stress and mitochondrial dysfunction. Melatonin pretreatment ameliorated myocardial injury by decreasing oxidative stress, restoring mitochondrial function, and inhibiting excessive mitophagy. However, ML221 or 3-TYP disrupted these beneficial effects of melatonin on I/R injury. Taken together, these results suggest that melatonin pretreatment ameliorates myocardial I/R injury through regulating the apelin/SIRT3 pathway to inhibit excessive mitophagy.
危险品化学品经营许可证（带存储）