摘要
目的研究地高辛对胰导管逆行注射牛磺胆酸钠诱导小鼠胆源性急性胰腺炎(ABP)的作用。方法将C57BL/6♂小鼠随机均分为空白对照组、模型组、地高辛组(0.05、0.1 mg·kg^(-1)地高辛)。小鼠经胰导管逆行注射3%牛磺胆酸钠,诱导ABP。术后1、3、6 h时,小鼠经腹腔注射地高辛溶液,模型组腹腔注射等量0.5%二甲亚砜生理盐水溶液。造模24 h后,将小鼠处死,采集小鼠血清,用于血液生化指标的检测;分离小鼠胰腺和肺组织,对其进行HE染色用于组织病理学分析;分离小鼠原代腺泡细胞,在体外用牛磺胆酸钠(5 mol·L^(-1))诱导坏死,并用碘化吡啶和Hoechst染色,直接评价地高辛对腺泡细胞坏死的影响。结果地高辛可显著抑制牛黄胆酸钠诱导的小鼠血清中淀粉酶、脂肪酶的升高,并改善小鼠胰腺和肺组织的病理变化,包括水肿、炎性浸润和局部坏死。同时,地高辛体外孵育可减轻牛磺胆酸钠诱导小鼠原代腺泡细胞的坏死。结论地高辛可减轻牛磺胆酸钠诱导小鼠的ABP和相关的肺损伤。
OBJECTIVE To explore the effect of Digoxin on acute biliary pancreatitis(ABP)in mice induced by retrograde injection of sodium taurocholate.METHODS C57BL/6 male mice were randomly divided into four groups:control group,model group,Digoxin with low dose(0.05 mg·kg^(-1))and Digoxin with high dose(0.1 mg·kg^(-1)).Mice were induced ABP by retrograde injection of 3%sodium taurocholate(4 mL·kg^(-1))through the pancreatic duct.Digoxin was given 1 h,3 h and 6 h after the surgery.Twenty-four hours after the surgery mice were sacrificed and serum was collected for amylase and lipase measurement.Pancreas and lung were separated for HE staining.Primary acinar cells were isolated and induced necrosis by sodium taurocholate(5 mol·L^(-1))and stained by Hoechst and propidium iodide(PI)for necrosis ratio test.RESULTS Digoxin significantly suppressed the raise of amylase and lipase as well as alleviated the histopathological injury of pancreas and lung such as edema,inflammation infiltration and necrosis.Digoxin could also inhibit the necrosis of acinar cells induced by sodium taurocholate in vitro.CONCLUSION Digoxin could improve acute biliary pancreatitis and associated lung injury.
作者
张晓雨
李世一
辛光
邢志华
钮海
黄文
ZHANG Xiaoyu;LI Shiyi;XIN Guang;XING Zhihua;NIU Hai;HUANG Wen(West China Hospital,Sichuan University,Sichuan University,Chengdu,Sichuan,610041 P.R.China;West China School of Pharmacy,Sichuan University,Chengdu,Sichuan,610041 P.R.China)
出处
《华西药学杂志》
CAS
CSCD
2021年第3期258-261,共4页
West China Journal of Pharmaceutical Sciences
基金
国家自然科学基金资助项目(批准号:81973580,81803866)
新药创制国家科技重大专项(编号:2019ZX09201005-005-001,2019ZX09201005-005-004)。