Mei Fangchao, Yu Jia, Li Man, Xiang Mingwei, Hong Yupu, Zhou Yu, You Yundong, Xia He, Jin Hongzhong, Wang Weixing
Dept of General Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China; Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Dept of General Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China; Hubei Key Laboratory of Digestive System Disease, Wuhan 430060, Hubei Province, China.
Pathol Res Pract. 2019 Jan;215(1):106-114. doi: 10.1016/j.prp.2018.10.030. Epub 2018 Oct 28.
For patients with acute necrotizing pancreatitis (ANP), a high body mass index (BMI) increases the likelihood of acute hepatic injury (AHI). In the current study, we explored whether magnesium isoglycyrrhizinate (MgIg) could alleviate ANP-induced liver injury in obese rats.
Sprague-Dawley (SD) rats were selected for the present study, and the ANP model was established by retrograde injection of 5% sodium taurocholate into the biliary-pancreatic duct. Thirty-six SD rats were randomly assigned to six groups: the normal (N), standard rat chow (SRC) normal (SN), SRC ANP (S-ANP), high-fat diet (HFD) normal (H-N), HFD ANP (H-ANP), and MgIg pretreatment HFD ANP (H-ANPT) groups. The rats in the H-ANPT group were treated with MgIg (30 mg/kg) intragastrically for 7 days before the ANP model was established. The rats were sacrificed 12 h after ANP was established, and the blood and pancreatic and liver tissues were collected. Differences in the physiology, pathology and cellular and molecular responses of the rats in each group were examined.
Analyses of serum amylase lipase, alanine aminotransferase and aspartate aminotransferase indicated that obesity aggravated ANP-induced hepatic injury and that MgIg improved liver function. The superoxide dismutase, malondialdehyde, M1 macrophage, M2 macrophage, neutrophil, NF-κB, IL-1β and caspase-3 levels in liver tissue showed that MgIg attenuated H-ANP-induced hepatic injury by inhibiting oxidative stress and inflammation.
Obesity aggravated ANP-induced liver injury via oxidative stress and inflammatory reactions. MgIg alleviated oxidative stress and decreased the inflammatory reaction, protecting the liver against the AHI induced by ANP in obese rats.
对于急性坏死性胰腺炎（ANP）患者，高体重指数（BMI）会增加急性肝损伤（AHI）的可能性。在本研究中，我们探讨了异甘草酸镁（MgIg）是否能减轻肥胖大鼠中ANP诱导的肝损伤。
本研究选用Sprague-Dawley（SD）大鼠，通过向胆胰管逆行注射5%牛磺胆酸钠建立ANP模型。36只SD大鼠随机分为六组：正常（N）组、标准大鼠饲料（SRC）正常（SN）组、SRC ANP（S-ANP）组、高脂饮食（HFD）正常（H-N）组、HFD ANP（H-ANP）组和MgIg预处理HFD ANP（H-ANPT）组。H-ANPT组的大鼠在建立ANP模型前7天经胃内给予MgIg（30 mg/kg）。在建立ANP模型12小时后处死大鼠，收集血液以及胰腺和肝脏组织。检测每组大鼠在生理、病理以及细胞和分子反应方面的差异。
血清淀粉酶、脂肪酶、丙氨酸转氨酶和天冬氨酸转氨酶分析表明，肥胖加重了ANP诱导的肝损伤且MgIg改善了肝功能。肝组织中超氧化物歧化酶、丙二醛、M1巨噬细胞、M2巨噬细胞、中性粒细胞、核因子κB、白细胞介素-1β和半胱天冬酶-3水平显示，MgIg通过抑制氧化应激和炎症减轻了H-ANP诱导的肝损伤。
肥胖通过氧化应激和炎症反应加重ANP诱导的肝损伤。MgIg减轻了氧化应激并降低了炎症反应，保护肝脏免受肥胖大鼠中ANP诱导的AHI。
