摘要
目的探讨富氢水(HRS)对脂多糖(LPS)诱导的小鼠脓毒症胰腺损伤的影响及可能机制。方法采用LPS尾静脉注射的方法建立小鼠脓毒症胰腺损伤模型。按随机数字表法将C57BL/6J雄性小鼠分为对照组、模型组(LPS组,LPS 5 mg/kg尾静脉注射)和HRS处理组(LPS+HRS组,LPS造模1 h后HRS 10 mL/kg腹腔注射),每组6只。制模后观察各组小鼠行为学表现,24 h后对各组小鼠进行胰腺组织苏木素伊红(HE)染色,并于显微镜下进行改良Schmidt组织病理学评分,酶联免疫吸附测定(ELISA)法检测血清淀粉酶含量、胰腺组织中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6、髓过氧化物酶(MPO)和丙二醛(MDA)水平。结果与对照相比,LPS组小鼠表现为嗜睡、寒战、行动迟缓,梳毛活动减少,并出现严重腹泻;胰腺组织出现水肿、炎性细胞浸润、出血和坏死,各项改良Schmidt组织病理学评分及总分升高;血清淀粉酶水平升高,胰腺组织中TNF-α、IL-6、MPO和MDA水平升高(均P<0.05)。与LPS组相比,LPS+HRS组小鼠嗜睡和寒战程度减轻、梳毛活动增加、腹泻减轻、排泄物减少;胰腺组织水肿、炎性细胞浸润、出血和坏死程度减轻,各项改良Schmidt组织病理学评分无明显变化(P>0.05),改良Schmidt组织病理学评分总分降低;血清淀粉酶水平,胰腺组织中TNF-α、IL-6、MPO和MDA水平显著降低,但仍高于对照组(均P<0.05)。结论富氢水可通过抑制炎症反应和减轻氧化应激改善LPS诱导的小鼠脓毒症胰腺损伤。
Objective To investigate the effect of hydrogen-rich saline(HRS)on endotoxin(LPS)-induced pancreatic injury in mice with sepsis and its possible mechanism.Methods The mouse model of pancreatic injury of sepsis was established by tail intravenous injection of LPS.Male C57BL/6J mice were randomly divided into 3 groups with 6 mice in each group.They were control group,model/LPS group(LPS 5 mg/kg tail vein injection)and HRS treatment/LPS+HRS group(HRS 10 mL/kg intraperitoneal injection 1 h after LPS modeling).After modeling,the behavioral manifestations were observed in three groups of mice.After 24 h,pancreatic tissue was stained with hematoxylin eosin(HE),and the modified Schmidt pancreas histopathological score was performed under microscope.The serum amylase,levels of tumor necrosis factor(TNF)-αand interleukin(IL)-6,myeloperoxidase(MPO)and malonaldehyde(MDA)in the pancreatic tissues were detected by enzyme-linked immunosorbent assay(ELISA).Results Compared with the control group,mice in the LPS group showed drowsiness,shivering,slow movement,less grooming activities and severe diarrhea.There were occurred edema,inflammatory cell infiltration,hemorrhage and necrosis in pancreatic tissues.The modified Schmidt histopathologic score increased.The serum amylase level increased,and TNF-α,IL-6,MPO and MDA levels in pancreatic tissues were also increased(P<0.05).Compared with the LPS group,the drowsiness and shivering were reduced,the combing activity was increased and diarrhea was alleviated with less excreta in the LPS+HRS group.The edema,inflammatory cell infiltration,hemorrhage and necrosis in pancreatic tissues were reduced in mice.There were no significant changes in the modified Schmidt histopathology scores between the two groups(P>0.05).The serum amylase level,and TNF-α,IL-6,MPO and MDA levels in the pancreas were significantly decreased,but which were still higher than those of control group(P<0.05).Conclusion HRS can significantly improve LPS-induced septic pancreatic injury in mice by inhibiting inflammatory response and alleviating oxidative stress.
作者
李悦娴
秦树存
张锦
LI Yue-xian;QIN Shu-cun;ZHANG Jin(Department of Anesthesiology,Shengjing Hospital of China Medical University,Shenyang 110004,China;Institute of Atherosclerosis,Shandong First Medical University,Taishan Hydrogen Biomedical Research Institute)
出处
《天津医药》
CAS
北大核心
2021年第8期808-812,共5页
Tianjin Medical Journal
基金
国家自然科学基金面上项目(81770855)
辽宁省沈阳市科技计划项目(17-230-9-45)。
关键词
脓毒症
胰腺疾病
氧化性应激
炎症
富氢水
胰腺损伤
sepsis
pancreatic diseases
oxidative stress
inflammation
hydrogen-rich saline
pancreatic injury