Nobiletin attenuates palmic acid-induced lipidosis in hepatocytes and regulatory mechanism of lncLSTR
10.3969/j.issn.1000-4718.2018.06.028
- VernacularTitle:川陈皮素对非酒精性脂肪肝细胞的保护作用和lncLSTR的调控机制
- Author:
Jiao WANG
1
;
Peng JIANG
;
Jian-Wei ZHOU
Author Information
1. 西南医科大学中西医结合学院
- Keywords:
Nobiletin;
Palmic acid;
Lipidosis;
Nonalcoholic fatty liver disease;
lncLSTR
- From:
Chinese Journal of Pathophysiology
2018;34(6):1129-1133,1137
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To observe the effects of nobiletin on palmic acid (PA)-induced lipidosis in hepatocytes and to discuss the regulatory mechanism of lncLSTR. METHODS:AML12 cells were cultured in vitro. The control group, PA group (0.2 mmol/L) and protection group (exposure to nobiletin at 1 mg/L, 5 mg/L, 15 mg/L or 50 mg/L for 2 h, fol-lowed by treatment with 0.2 mmol/L PA) were established according to the experimental requirements. The lipid accumula-tion was morphologically observed by Oil red O staining in the cells. The qPCR was applied to detect mRNA expression, and the protein expression was determined by and Western blot. RESULTS:PA treatment (0.2 mmol/L) induced lipidosis, while 50 mg/L nobiletin pretreatment suppressed the lipidosis. Compared with control group, the mRNA expression of Apoc2 in PA group was significantly down-regulated (P<0.05), but increased by nobiletin pretreatment compared with PA group (P<0.05). The protein expression of Apoc2 in PA group was significantly down-regulated (P<0.05), but increased by nobiletin pretreatment (P<0.05). The expression of lncLSTR in PA group was significantly increased (P<0.05) and that was inhibited by nobiletin pretreatment (P<0.05). A negative correlation between Apoc2 protein and lncLSTR expression in PA group (R2=0.717 9, P<0.01) was observed. A negative correlation between Apoc2 protein and lncLSTR expression in protection group (R2=0.525 3, P<0.05) was also found. CONCLUSION:Nobiletin has anti-lipidosis effect on hepa-tocytes. The mechanism is partially related to the inhibition of up-regulation of lncLSTR, thus down-regulating Apoc2 expres-sion.
