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目的研究人参皂苷预处理对内毒素(脂多糖)所致急性肺损伤(ALI)大鼠的保护机制。方法按雌雄对半将成年大鼠按体重随机分为4组(每组10只):空白组、模型组、人参皂苷组和对照组。造模前3天,人参皂苷组腹腔注射人参皂苷100 mg·kg~(-1),每天1次,连用3 d;造模前1天,对照组腹腔注射甲强龙40 mg·kg~(-1)。空白组给与等量的0.9%Na Cl。3组均(空白组以外)腹腔注射脂多糖5 mg·kg~(-1)复制大鼠ALI模型。检测大鼠R动脉血氧合指数(PO_2/FiO_2)与肺泡灌洗液(BALF)中蛋白含量,用ELLISA检测大鼠BALF中肿瘤坏死因子α(TNF-α)和白细胞介素-6(IL-6)和白细胞介素-10(IL-10)表达水平。结果 PaO_2/FiO_2:与空白组的(485.49±20.71)mmHg比较,模型组为(269.29±13.61)mmHg,差异有统计学意义(P<0.01)。与模型组比较,人参皂苷组和对照组分别为(379.74±15.06),(398.08±16.89)mmHg,差异均有统计学意义(均P<0.01)。BALF中蛋白含量:与空白组的(39.00±5.00)μg·mL~(-1)比较,模型组为(3.69±3.86)μg·mL~(-1),差异有统计学意义(P<0.01)。与模型组比较,人参皂苷组和对照组分别为(77.00±6.00),(97.00±11.00)μg·mL~(-1),差异均有统计学意义(均P<0.01)。BALF中TNF-α、IL-6和IL-10水平:与空白组的(218.85±7.36),(10.84±1.66),(50.00±7.21)ng·L~(-1)比较,模型组分别为(505.78±7.60),(61.55±4.08),(94.76±3.58)ng·L~(-1),差异均有统计学意义(均P<0.01)。与模型组比较,人参皂苷组和对照组分别为(346.42±11.24),(338.14±5.37)ng·L~(-1);(42.49±1.26),(40.07±2.60)ng·L~(-1);(114.22±2.58),(119.07±4.08)ng·L~(-1),差异均有统计学意义(均P<0.01)。结论人参皂苷可能通过上调IL-10的表达及下调TNF-α与IL-6的表达来保护大鼠的急性肺损伤。
Objective To study the protective mechanism of ginsenoside preconditioning on acute lung injury (ALI) induced by endotoxin (lipopolysaccharide) in rats. Methods According to body weight, male and female adult rats were randomly divided into 4 groups (10 in each group): blank group, model group, ginsenoside group and control group. Three days before modeling, ginsenoside group was intraperitoneally injected with 100 mg · kg -1 of ginsenoside once daily for 3 d. One day before model control, the control group received intraperitoneal injection of 40 mg · kg ~ (-1) of methylprednisolone -1). The blank group was given the same amount of 0.9% NaCl. All rats in the 3 groups (except the blank group) were intraperitoneally injected with lipopolysaccharide 5 mg · kg -1 for ALI model. The content of protein in arterial oxygenation index (PO_2 / FiO_2) and alveolar lavage fluid (BALF) of rats was measured. The levels of tumor necrosis factor α (TNF-α) and interleukin-6 -6) and interleukin-10 (IL-10) expression levels. Results PaO2 / FiO2: Compared with the blank group (485.49 ± 20.71) mmHg, the model group was (269.29 ± 13.61) mmHg, the difference was statistically significant (P <0.01). Compared with the model group, the ginsenoside group and the control group were (379.74 ± 15.06), (398.08 ± 16.89) mmHg, the differences were statistically significant (all P <0.01). Compared with the blank group (39.00 ± 5.00) μg · mL -1, the protein level in BALF was (3.69 ± 3.86) μg · mL -1 in the model group, with significant difference (P <0.01) ). Compared with the model group, the concentrations of ginsenoside and control group were (77.00 ± 6.00) and (97.00 ± 11.00) μg · mL -1, respectively (all P <0.01). Compared with the blank group (218.85 ± 7.36), (10.84 ± 1.66) and (50.00 ± 7.21) ng · L -1, the levels of TNF-α, IL-6 and IL-10 in BALF were (505.78 ± 7.60), (61.55 ± 4.08) and (94.76 ± 3.58) ng · L -1, respectively (all P <0.01). Compared with the model group, the ginsenoside group and the control group were (346.42 ± 11.24), (338.14 ± 5.37) ng · L -1, (42.49 ± 1.26) and (40.07 ± 2.60) ng · L -1 1), (114.22 ± 2.58) and (119.07 ± 4.08) ng · L -1, respectively (all P <0.01). Conclusion Ginsenoside may protect rats from acute lung injury by up-regulating the expression of IL-10 and down-regulating the expressions of TNF-α and IL-6.