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目的研究红芪总多糖对内毒素(LPS)诱导的急性肺损伤(ALI)的保护作用。方法按照体重将72只小鼠随机分为6组(每组12只):正常组、模型组、对照组及3个剂量实验组。正常组注射等体积量0.9%Na Cl,其余各组腹腔注射10 mg·kg~(-1)LPS,建立小鼠肺损伤模型。在造模后4 h,3个剂量(50,100,200 mg·kg~(-1))实验组每日分别灌服红芪总多糖,对照组每日灌服3 mg·kg~(-1)地塞米松,正常组与模型组每日每只给予0.9%Na Cl,连续3 d。以酶联免疫吸附实验测定肿瘤坏死因子-α(TNF-α)、白细胞介素~(-1)0(IL~(-1)0)表达,用分光光度法检测血清总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)及丙二醛(MDA)含量,以单细胞凝胶电泳检测小鼠淋巴细胞DNA损伤。结果给药后,与模型组小鼠血清TNF-α、IL~(-1)0含量分别为(156.23±7.39),(44.24±2.89)ng·L~(-1)相比,中、大2个剂量实验组的TNF-α、IL~(-1)0含量分别为(139.45±6.57),(35.30±1.88);(120.13±6.81),(33.11±2.71)ng·L~(-1),差异均有统计学意义(均P<0.01)。与模型组小鼠血清T-AOC、SOD水平分别为(5.56±0.13),(67.68±4.86)U·mg~(-1)比较,中、大2个剂量实验组的T-AOC、SOD水平分别为(5.91±0.10),(70.00±3.04);(6.10±0.09),(76.21±4.03)U·mg~(-1),差异均有统计学意义(均P<0.01)。与模型组小鼠血清MDA含量(5.55±0.11)nmol·mg~(-1)相比,中、大2个剂量实验组的MDA含量分别为(5.01±0.11),(4.17±0.12)nmol·mg~(-1),差异均有统计学意义(均P<0.01)。与模型组的小鼠外周血淋巴细胞DNA尾长、尾矩及Olive尾矩分别为(6.45±0.08),(3.22±0.14),(3.35±0.12)μm相比,中、大2个剂量实验组的DNA尾长、尾矩及Olive尾矩分别为(5.81±0.10),(5.24±0.10);(2.86±0.12),(2.71±0.16);(2.67±0.10),(2.17±0.18)μm,差异均有统计学意义(均P<0.01)。结论红芪总多糖对LPS引起的急性肺损伤具有保护作用。其作用机制可能与调节促炎因子TNF-α和抗炎因子IL~(-1)0比例失衡,调节氧化和抗氧化的平衡有关。
Objective To study the protective effect of total polysaccharide of Radix Hedysari on acute lung injury (ALI) induced by endotoxin (LPS). Methods According to body weight, 72 mice were randomly divided into 6 groups (12 in each group): normal group, model group, control group and 3 dose experimental groups. The rats in normal group were injected 0.9% sodium chloride (Na Cl) in equal volume and the other groups were injected intraperitoneally with LPS (10 mg · kg -1) to establish a mouse model of lung injury. At 4 h after model establishment, the experimental groups of three doses (50, 100 and 200 mg · kg -1) were given total polysaccharide of Radix Hedysari daily, while the control group was given 3 mg · kg -1 of dextrose In the control group, 0.9% NaCl was given daily to the normal group and model group for 3 days. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1 (-1) 0 were detected by enzyme-linked immunosorbent assay (ELISA) -AOC), superoxide dismutase (SOD) and malondialdehyde (MDA) were detected by single cell gel electrophoresis. Results After administration, the levels of TNF-α and IL-1 0 in model group were (156.23 ± 7.39) and (44.24 ± 2.89) ng · L -1, The contents of TNF-α and IL-1 0 in the two experimental groups were (139.45 ± 6.57), (35.30 ± 1.88), (120.13 ± 6.81), (33.11 ± 2.71) ng · L -1 ), The differences were statistically significant (all P <0.01). Compared with model group, serum levels of T-AOC and SOD were (5.56 ± 0.13) and (67.68 ± 4.86) U · mg -1, respectively. T-AOC and SOD levels in the middle and large dose groups (5.91 ± 0.10), (70.00 ± 3.04), (6.10 ± 0.09) and (76.21 ± 4.03) U · mg ~ (-1), respectively. The differences were statistically significant (all P <0.01). Compared with the model group, the content of MDA in the experimental group was (5.01 ± 0.11) and (4.17 ± 0.12) nmol · mg ~ (-1), the differences were statistically significant (all P <0.01). The DNA tail length, tail moment and Olive tail moment of mouse peripheral blood lymphocytes in the model group were (6.45 ± 0.08), (3.22 ± 0.14) and (3.35 ± 0.12) μm, respectively. The tail length, tail moment and Olive tail moment were (5.81 ± 0.10), (5.24 ± 0.10), (2.86 ± 0.12), (2.71 ± 0.16), (2.67 ± 0.10), (2.17 ± 0.18) μm , The differences were statistically significant (all P <0.01). Conclusion Total polysaccharide of Radix Hedysari can protect LPS-induced acute lung injury. Its mechanism may be related to the imbalance between the regulation of proinflammatory cytokines TNF-α and IL-1 0, and the regulation of oxidation and antioxidation.