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目的探讨吉林人参低聚肽减轻大鼠慢性炎症作用及机制。方法将大鼠随机分为5组,分别为对照组和62.5、125.0、250.0、500.0 mg/kg人参组,分别灌胃给予蒸馏水和相应浓度的吉林人参低聚肽,每天1次,连续30 d。采用棉球植入法计算棉球肉芽肿净重量、酶联免疫法检测大鼠血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、IL-10、一氧化氮(NO)和前列腺素E2(PGE2)水平。结果与对照组比较[(0.248±0.038)g],250.0 mg/kg人参组大鼠肉芽肿净重量[(0.162±0.047)g]下降(P<0.05),呈一定剂量效应关系;对照组大鼠血清中TNF-α、IL-1β、IL-10、PGE2水平及NO含量分别为(309.9±16.1)、(46.2±2.6)、(30.4±3.1)、(354.2±10.2)ng/L与(36.2±3.1)μmol/L,250.0 mg/kg人参组大鼠血清中TNF-α、IL-1β、IL-10、PGE2水平及NO含量分别为(202.4±17.3)、(21.4±2.4)、(68.4±3.9)、(438.6±16.3)ng/L与(31.5±2.5)μmol/L;与对照组比较,250.0mg/kg人参组大鼠血清中TNF-α、IL-1β与NO水平下降,IL-10、PGE2水平升高(P<0.05)。结论吉林人参低聚肽能够减轻大鼠慢性炎症反应,其机制可能与其降低促炎因子水平、升高抗炎因子水平有关。
Objective To investigate the effect and mechanism of Jilin ginseng oligopeptide on relieving chronic inflammation in rats. Methods The rats were randomly divided into 5 groups: control group and 62.5, 125.0, 250.0 and 500.0 mg / kg ginseng groups, respectively, and distilled water and corresponding concentrations of Jilin ginseng oligopeptide were administered orally, once daily for 30 days . The weight of granuloma of cotton balls was calculated by cotton ball implanting method. The contents of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) Nitric oxide (NO) and prostaglandin E2 (PGE2) levels. Results Compared with the control group [(0.248 ± 0.038) g], the net weight of granulomas in 250.0 mg / kg ginseng group decreased significantly (P <0.05), and the dose-dependent The levels of TNF-α, IL-1β, IL-10, PGE2 and NO in rat serum were (309.9 ± 16.1), (46.2 ± 2.6), (30.4 ± 3.1), (354.2 ± 10.2) ng / The levels of TNF-α, IL-1β, IL-10, PGE2 and NO in the serum of 250.0 mg / kg ginseng group were (202.4 ± 17.3), (21.4 ± 2.4) and 68.4 ± 3.9), (438.6 ± 16.3) ng / L and (31.5 ± 2.5) μmol / L respectively. Compared with the control group, the levels of TNF-α, IL-1β and NO in the serum of 250.0mg / IL-10, PGE2 levels increased (P <0.05). Conclusion Jilin ginseng oligopeptide can reduce the chronic inflammation in rats, and its mechanism may be related to the decrease of the level of proinflammatory cytokines and the elevation of anti-inflammatory cytokines.