Sodium benzoate induces pancreatic inflammation and β-cell apoptosis via benzoylation modification
10.3760/cma.j.cn311282-20231229-00237
- VernacularTitle:苯甲酸钠通过苯甲酰化诱导胰腺炎症和β细胞凋亡
- Author:
Dongze LI
1
;
Li ZHANG
;
Yanqiu HE
;
Tingting ZHOU
;
Chenlin GAO
;
Pijun YAN
;
Zongzhe JIANG
;
Yang LONG
;
Qin WAN
;
Wei HUANG
;
Yong XU
Author Information
1. 西南医科大学附属医院内分泌与代谢内科，泸州 646000
- Keywords:
Sodium benzoate;
Benzoylation;
Inflammation;
Apoptosis;
Insulin
- From:
Chinese Journal of Endocrinology and Metabolism
2024;40(5):427-435
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore whether the food additive sodium benzoate(NAB) induces pancreatic inflammation and β cell apoptosis through the benzoylation(Kbz) modification pathway.Methods:In vivo experiments: C57BL/6J male mice(8 weeks old, 18-20 g) were randomly divided into normal control group(double distilled water feeding) and NAB feeding group(1 g/kg NAB feeding). Blood glucose were measured. After 20 weeks, fasting serum insulin, interleukin(IL)-18, IL-1β, and benzoyl-CoA levels were detected by ELISA method. Bax, IL-18, Pan-Kbz and Pan-Kac were detected by immunohistochemistry staining. In vitro experiments: β-TC-6 cells were cultured with NAB(6 mmol/L) or benzoyl-CoA(100 μmol/L) as stimulator and acyltransferase P300 inhibitor A485(10 μmol/L) as intervention factor. 24 hours later, inflammation, apoptosis, insulin secretion and Pan-Kbz level were detected by qRT-PCR, ELISA and Western blotting.Results:In the in vivo experiments, compared to the NC group, mice in the NAB group exhibited impaired glucose tolerance, decreased fasting insulin levels, significantly increased serum benzoyl coenzyme A concentrations, relatively elevated pancreatic IL-1β, IL-18, and Bax protein expressions, increased levels of Pan-Kbz, while Pan-Kac levels were downregulated(all P<0.05); In vitro experiments, NAB dose-dependently inhibited insulin secretion, promoted the release of Pan-Kbz and inflammatory factors IL-18 and TNF- α, inhibited Bcl-2 expression and up-regulated Bax expression, A485 reversed NAB-induced Pan-Kbz modification, improved NAB-induced inflammation and apoptosis, and promoted insulin secretion(all P<0.05). Conclusion:NAB may induce pancreatic inflammation, β-cell apoptosis, and impair insulin secretion through Kbz modification pathway.
