火棘多糖对CCl_4所致大鼠肝损伤保护作用

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目的探讨火棘多糖对四氯化碳(CCI_4)所致大鼠肝损伤的保护作用。方法将50只Wistar大鼠随机分为5组:对照组,CCI_4模型组,联苯双酯(BP)组,火棘多糖200、400 mg/kg组。对照组大鼠中腹膜下注射橄榄油,其余各组大鼠腹膜下注射30%CCI_4,联苯双酯组、火棘多糖组分别灌胃BP 200 mg/kg,火棘多糖200、400 mg/kg。5周后,测定血清中丙氨酸转氨酶(ALT)及天冬氨酸转氨酶(AST)含量;检测肝组织中丙二醛、谷胱甘肽过氧化物酶(GSH-Px)含量及总抗氧化能力(T-AOC)活性;用real time PCR检测大鼠肝组织中核因子相关因子2(Nrf2)及过氧化氢酶(CAT)mRNA表达变化。结果与CCI_4模型组大鼠血清ALT、AST含量[(521.42±68.21)、(589.17±39.44)U/L]比较,火棘多糖200、400 mg/kg组大鼠血清ALT、AST含量[分别为(221.13±28.46)、(190.31±27.32)与(286.4±31.57)、(224.6±30.52)U/L]明显降低,差异有统计学意义(P<0.05);与CCI_4模型组大鼠肝组织中丙二醛含量[(32.14±3.26)nmol/mg pro]比较,火棘多糖200、400 mg/kg组大鼠肝组织中丙二醛含量[分别为(23.29±4.38)、(18.67±3.28)nmol/mg pro]明显降低,差异有统计学意义(P<0.05);与CCI_4模型组大鼠肝组织中T-AOC活性[(73.15±9.23)U/m L]比较,火棘多糖200、400 mg/kg组大鼠肝组织中T-AOC活性[分别为(106.32±14.23)、(152.31±16.12)U/m L]明显升高,差异有统计学意义(P<0.05);real time PCR结果显示,与CCI_4模型组比较,火棘多糖组大鼠肝组织中Nrf2及CAT mRNA表达水平增加。结论火棘多糖对CCI_4所致大鼠肝损伤具有保护作用,其机制可能与火棘多糖可提高大鼠抗氧化能力有关。 Objective To investigate the protective effect of Pyracantha fortuneana against liver injury induced by carbon tetrachloride (CCI_4) in rats. Methods Fifty Wistar rats were randomly divided into five groups: control group, CCI 4 model group, bifendate group, and Pyracantha fortuneana group 200 and 400 mg / kg. The rats in the control group were injected subperitoneally with olive oil. The rats in other groups were injected intraperitoneally with 30% CCI_4, bifendate group and pyracantha polysaccharide group respectively with 200 mg / kg and 200,400 mg / kg. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) contents were measured after 5 weeks. The levels of malondialdehyde, glutathione peroxidase (GSH-Px) (T-AOC). The mRNA expressions of Nrf2 and CAT in rat liver tissues were detected by real time PCR. Results Compared with CCI 4 model group, serum ALT and AST levels [(521.42 ± 68.21) and (589.17 ± 39.44) U / L] (221.13 ± 28.46), (190.31 ± 27.32) and (286.4 ± 31.57) and (224.6 ± 30.52) U / L, respectively, and the difference was statistically significant (P <0.05) Compared with the control group, the content of malondialdehyde (MDA) in the liver tissue of [(32.24 ± 3.26) nmol / mg pro] groups was (23.29 ± 4.38, 18.67 ± 3.28, (P <0.05). Compared with the T-AOC activity in hepatic tissue of CCI 4 model group [(73.15 ± 9.23) U / m L] The T-AOC activity in the liver of 400 mg / kg group (106.32 ± 14.23 and 152.31 ± 16.12 U / m L, respectively) was significantly higher than that of the control group (P <0.05) PCR results showed that compared with CCI_4 model group, the expression levels of Nrf2 and CAT mRNA in the liver tissue of Pyracantha fortuneana group increased. Conclusions Pyracantha fortuneana polysaccharides can protect rat liver injury induced by CCI_4, and its mechanism may be related to the fact that Pyracantha fortuneana polysaccharides can improve antioxidant capacity of rats.
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