本文選題：小牛血去蛋白提取物 + 四氯化碳��； 參考：《北華大學(xué)》2017年碩士論文

【摘要】：目的:觀察小牛血去蛋白提取物(deproteinized extract of calf blood,DECB)對(duì)化學(xué)性肝損傷小鼠的保護(hù)作用,并初步探討其作用機(jī)制。方法:建立兩種小鼠急性肝損傷模型,分別為酒精致急性肝損傷模型和CCl4致急性肝損傷模型。酒精性肝損傷實(shí)驗(yàn),取健康ICR種小鼠60只,隨機(jī)分組法分為:空白組、模型組、陽性藥物組和高活性小牛血去蛋白提取物低、中、高劑量組,每組10只。灌胃給藥,空白組給予生理鹽水20 m L·kg-1,DECB低、中和高劑量組分別給予DECB 0.25、0.50、1.00 g·kg-1,陽性藥物組給予護(hù)肝片0.63g·kg-1。每天1次,連續(xù)30d,末次給藥1 h后,除空白組外,其他各組一次性給予50%乙醇14 m L·kg-1,并禁食16 h建立急性酒精性肝損傷模型。測(cè)定小鼠的耐受酒精時(shí)間和醉酒時(shí)間,檢測(cè)血清中丙氨酸轉(zhuǎn)氨酶(ALT)和天冬氨酸轉(zhuǎn)氨酶(AST)活性,檢測(cè)肝組織中甘油三酯(TG)、谷胱甘肽(GSH)和丙二醛(MDA)水平,并進(jìn)行肝組織病理切片檢查。CCl4致急性肝損傷實(shí)驗(yàn),取健康ICR種小鼠40只,隨機(jī)分組法分為空白組、模型組、陽性藥物組和DECB組每組10只。各組小鼠灌胃給藥,空白組給予生理鹽水20 m L·kg-1,DECB組給予DECB 1.00g·kg-1,陽性藥物組給予護(hù)肝片0.63g·kg-1。每天1次,連續(xù)30d;末次給藥2 h后,對(duì)照組小鼠腹腔注射調(diào)和油溶液,其余各組小鼠腹腔注射10%CCl4調(diào)和油溶液(10 m L·kg-1)并禁食,建立CCl4致急性肝損傷模型。測(cè)定各組小鼠血清丙氨酸氨基轉(zhuǎn)移酶(ALT)、天冬氨酸氨基轉(zhuǎn)移酶(AST)活性和肝組織總超氧化物歧化酶(T-SOD)、谷胱甘肽(GSH)及丙二醛(MDA)水平;HE染色法觀察肝組織病理改變,TUNEL方法檢測(cè)肝組織細(xì)胞凋亡,通過m RNA表達(dá)芯片篩選DECB組和模型組的差異表達(dá)基因及其相關(guān)通路。結(jié)果:酒精性肝損傷實(shí)驗(yàn)發(fā)現(xiàn),與模型組比較,DECB組明顯減輕小鼠醉酒癥狀,DECB高劑量組和陽性藥組小鼠酒精耐受時(shí)間延長(P0.05㖞,醉酒時(shí)間縮短(P0.05㖞;DECB中、高劑量組小鼠血清ALT和AST活性均明顯低于模型組(P0.05㖞;與模型組比較,DECB中、高劑量組和陽性藥物組小鼠肝組織中MDA和TG水平明顯降低,差異有統(tǒng)計(jì)學(xué)意義(P0.05㖞;與模型組比較,DECB高劑量組小鼠乙醇所致肝組織病理學(xué)損傷明顯減輕。CCl4致急性肝損傷實(shí)驗(yàn)發(fā)現(xiàn)DECB組小鼠血清ALT和AST活性均明顯低于模型組(P0.05㖞;與模型組比較,DECB組小鼠肝組織MDA和GSH水平明顯降低(P0.05㖞,T-SOD水平明顯升高(P0.05㖞;肝組織病理學(xué)損傷明顯減輕,凋亡指數(shù)降低(P0.05㖞;在聚類結(jié)果中發(fā)現(xiàn)細(xì)胞凋亡通路中共有9個(gè)差異表達(dá)基因,2個(gè)基因表達(dá)上調(diào),7個(gè)基因表達(dá)下調(diào)。結(jié)論:DECB對(duì)化學(xué)性肝損傷具有保護(hù)作用,可以增強(qiáng)肝臟抗氧化能力,抑制肝細(xì)胞凋亡,其機(jī)制可能與調(diào)控細(xì)胞凋亡通路基因表達(dá)有關(guān)。
[Abstract]:Objective: to observe the protective effect of deproteinized extract of calf blood extract (DECB) on chemically induced liver injury in mice, and to explore its mechanism. Methods: two kinds of acute liver injury models were established in mice, which were acute liver injury induced by alcohol and CCL _ 4, respectively. In alcoholic liver injury experiment, 60 ICR mice were randomly divided into blank group, model group, positive drug group and high active calf blood deproteinization extract with 10 rats in each group. The normal saline 20 mL kg -1 DECB was given to the blank group, the middle and high dose groups were given the DECB 0.25 ~ 0.50 ~ 0.50 g 路kg ~ (-1) respectively, and the positive drug group was given 0.63 g 路kg ~ (-1) of protective liver tablet. Once a day for 30 days, after the last administration for 1 hour, the other groups were given 50% ethanol 14ml 路kg -1 for one time, and fasting for 16 h to establish the model of acute alcoholic liver injury. The alcohol tolerance time and drunkenness time of mice were measured. The activities of alanine aminotransferase (alt) and aspartate aminotransferase (AST) in serum and the levels of triglyceride, glutathione (GSH) and malondialdehyde (MDAs) in liver tissue were measured. 40 ICR mice were randomly divided into blank group, model group, positive drug group and DECB group. Mice in each group were given intragastric administration of DECB 1.00 g kg-1in the blank group and 0.63 g kg-1 in the positive drug group. The control group was given normal saline 20 mL 路kg ~ (-1) 路kg ~ (-1) and the positive drug group was given 0.63 g / kg ~ (-1). After the last administration for 2 hours, the control mice were injected with the blending oil solution intraperitoneally, and the other mice were injected intraperitoneally with the 10l4 blend oil solution 10 mL kg-1) and fasted to establish the model of acute liver injury induced by CCl4. The activity of serum alanine aminotransferase (alt), aspartate aminotransferase (AST), total superoxide dismutase (T-SOD), glutathione (GSH) and malondialdehyde (MDA) were measured in each group of mice. Detection of apoptosis in liver tissue, The differentially expressed genes and their related pathways in DECB group and model group were screened by mRNA expression microarray. Results: compared with the model group, the alcoholic liver injury test showed that the alcohol tolerance time of the DECB group and the positive drug group were significantly reduced compared with the model group, and the alcohol tolerance time was prolonged in the DECB group and the positive drug group, and the alcohol tolerance time was shortened in the DECB group, the alcohol tolerance time was shortened in the DECB group, and the alcohol tolerance time was shortened in the DECB group. The activities of alt and AST in high dose group were significantly lower than those in model group (P 0.05), and the levels of MDA and TG in liver tissue of mice in high dose group and positive drug group were significantly lower than those in model group. Compared with the model group, the liver histopathological damage induced by ethanol in the DECB group was significantly reduced. The serum alt and AST activities in the DECB group were significantly lower than those in the model group, and those in the DECB group were significantly lower than those in the model group. Compared with the model group, the levels of MDA and GSH in the liver tissue of the DECB group decreased significantly, the level of P0.05TSOD increased significantly, and the pathological damage of the liver tissue was alleviated obviously. The results of cluster analysis showed that there were 9 differentially expressed genes, 2 up-regulated genes and 7 down-regulated genes in the apoptotic pathway. Conclusion DECB has protective effect on chemically induced liver injury. It can enhance the antioxidant ability of liver and inhibit the apoptosis of hepatocytes. The mechanism may be related to the regulation of gene expression of apoptosis pathway.
【學(xué)位授予單位】：北華大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R965

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