Melatonin Alleviates Liver Apoptosis in Bile Duct Ligation Young Rats.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
Bile duct ligation (BDL) | increase | cholestasis and liver damages | rats | - | displayed | #1 |
Bile duct ligation (BDL) | increase | liver apoptosis | young male Sprague-Dawley rats | - | showed | #2 |
Bile duct ligation (BDL) | increase | pro-inflammatory mediators | young male Sprague-Dawley rats | - | increased | #3 |
Bile duct ligation (BDL) | increase | caspases alterations | young male Sprague-Dawley rats | - | caused | #4 |
Bile duct ligation (BDL) | increase | anti-apoptotic factors changes | young male Sprague-Dawley rats | - | caused | #5 |
Bile duct ligation (BDL) | increase | dysfunction of ER homeostasis | young male Sprague-Dawley rats | - | caused | #6 |
melatonin | decrease | apoptosis | young male Sprague-Dawley rats | - | effectively reversed | #7 |
melatonin | decrease | ER stress | young male Sprague-Dawley rats | - | reversed | #8 |
melatonin | decrease | apoptosis | HepG2 cells | - | exerted its effect | #9 |
Bile duct ligation (BDL) | increase | liver apoptosis | young rats | - | caused | #10 |
melatonin | decrease | apoptotic changes | young rats | - | rescued | #11 |
melatonin | decrease | ER stress | young rats | - | reversed | #12 |
Bile duct ligation (BDL)-treated rats display cholestasis and liver damages. The potential protective activity of melatonin in young BDL rats in terms of apoptosis, mitochondrial function, and endoplasmic reticulum (ER) homeostasis has not yet been evaluated. Three groups of young male Sprague-Dawley rats were used: one group received laparotomy (Sham), a second group received BDL for two weeks (BDL), and a third group received BDL and intraperitoneal melatonin (100 mg/day) for two weeks (BDL + M). BDL group rats showed liver apoptosis, increased pro-inflamamtory mediators, caspases alterations, anti-apoptotic factors changes, and dysfunction of ER homeostasis. Melatonin effectively reversed apoptosis, mainly through intrinsic pathway and reversed ER stress. In addition, in vitro study showed melatonin exerted its effect mainly through the melatonin 2 receptor (MT2) in HepG2 cells. In conclusion, BDL in young rats caused liver apoptosis. Melatonin rescued the apoptotic changes via the intrinsic pathway, and possibly through the MT2 receptor. Melatonin also reversed ER stress induced by BDL.