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目的:探讨人参皂苷Rh2对支气管哮喘小鼠气道重塑及VEGF和MMP-9信号通路的影响。方法:60只清洁级雌性BABL/c小鼠,随机数字表法分为6组,每组10只,分别为A组为生理盐水对照组、B组为卵蛋白(OVA)哮喘组、C组为人参皂苷Rh2低剂量组、D组人参皂苷Rh2高剂量组、E组为SU5416治疗组、F组为地塞米松治疗组。在末次激发24h后所有小鼠取左肺组织行苏木精-伊红(HE)染色、Masson三色染色、PAS染色。取右肺组织分别用酶联免疫吸附法(ELISA),RT-PCR和Westernblot检测支气管肺泡灌洗液(BALF)中IL-4、IL-5、IL-13含量以及VEGF和MMP-9 mRNA、蛋白表达。结果:哮喘模型组小鼠与对照组相比较BALF中炎症细胞计数、IL-4、IL-5、IL-13水平增高;肺组织VEGF和MMP-9 mRNA、蛋白表达水平均显著高于对照组(P<0.01)。人参皂苷Rh2干预组小鼠与哮喘模型组相比较BALF中炎症细胞计数、IL-4、IL-5、IL-13水平,VEGF和MMP-9 mRNA、蛋白表达水平均显著降低,具有显著差异(P<0.01),但2个不同治疗组之间上述各指标间差异无统计学意义(P>0.05)。结论:人参皂苷Rh2可抑制哮喘小鼠气道重塑的发生,其机制有可能部分是通过抑制VEGF/MMP-9信号通路而实现的。
Objective: To investigate the effects of ginsenoside Rh2 on airway remodeling and VEGF and MMP-9 signaling in bronchial asthma mice. Methods: Sixty clean female BABL / c mice were randomly divided into six groups (n = 10 in each group): group A was saline control group, group B was ovalbumin (OVA) asthma group, group C Ginsenoside Rh2 low dose group, D group ginsenoside Rh2 high dose group, E group SU5416 treatment group, F group dexamethasone treatment group. Left hind lung tissue was stained with hematoxylin and eosin (HE), Masson trichrome and PAS in all mice 24h after the last challenge. The contents of IL-4, IL-5 and IL-13 and the expressions of VEGF and MMP-9 mRNA in bronchoalveolar lavage fluid (BALF) were determined by enzyme linked immunosorbent assay (ELISA), RT- Protein. Results: Compared with the control group, the number of inflammatory cells in BALF and the levels of IL-4, IL-5 and IL-13 in asthmatic model group were increased. The levels of VEGF and MMP-9 mRNA and protein in lung tissue were significantly higher than those in control group (P <0.01). Compared with asthmatic model group, ginsenoside Rh2 intervention group had significantly lower inflammatory cell counts, IL-4, IL-5, IL-13, VEGF and MMP-9 mRNA and protein expression in BALF P <0.01). However, there was no significant difference between the two groups (P> 0.05). CONCLUSION: Ginsenoside Rh2 can inhibit the airway remodeling in asthmatic mice. The mechanism may be partly through the inhibition of VEGF / MMP-9 signaling pathway.