金丝桃苷抑制肺炎支原体肺炎模型小鼠的损伤

Hyperoside suppresses injury in Mycoplasma pneumoniae pneumonia mice

目的:探讨金丝桃苷对肺炎支原体肺炎(MPP)小鼠的保护作用及其调控机制。方法:选取BALB/c小鼠40只,随机分为对照组、模型组、金丝桃苷低剂量(12.5 mg/kg)组和金丝桃苷高剂量(50 mg/kg)组。以肺炎支原体国际标准株(MPFH)滴鼻造模,第2天开始治疗,治疗3 d后进行后续实验。HE染色检测肺组织病理改变;全自动生化分析仪检测血清中C-反应蛋白(CRP)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、乳酸脱氢酶(LDH)和心肌型肌酸激酶同工酶(CK-MB)水平,检测肺组织中活性氧簇(ROS)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)水平;ELISA和Western blot方法分别检测血清和肺组织中白细胞介素1β(IL-1β)、IL-6、IL-18和肿瘤坏死因子α(TNF-α)水平;RT-q PCR和Western blot方法检测NLRP3、ASC和caspase-1的mRNA和蛋白表达。结果:与对照组相比,模型组小鼠的肺组织中出现炎症反应、肺泡间质增宽等病理变化;CRP、ALT、AST、LDH和CK-MB水平显著上调(P<0.05);ROS水平显著上升,而SOD和GSH水平显著下降(P<0.05);IL-1β、IL-6、IL-18和TNF-α水平显著上调(P<0.05);NLRP3、ASC和caspase-1的蛋白表达也显著升高(P<0.05)。与模型组相比,金丝桃苷组中的上述症状明显减轻,且高剂量比低剂量组的缓解效果更明显。结论:金丝桃苷能够抑制MPP小鼠的损伤,这可能与其抑制氧化应激和NLRP3炎性体的激活有关。

AIM： To investigate the protective effect of hyperoside （Hyp） on Mycoplasma pneumoniae （MP） pneumonia （MPP） mice and the underlying regulatory mechanism.METHODS： BALB/c mice （n=40） were randomly divided into control group, model group, low-dose （12.5 mg/kg） Hyp group and high-dose （50 mg/kg） Hyp group. The MPP model was established using MP standard strains （MPFH） through nasal dripping. The treatment started on the second day, and the follow-up experiments were performed after 3 d. The lung histopathology were detected by HE staining. The levels of C-reactive protein （CRP）, alanine aminotransferase （ALT）, aspartate transaminase （AST）, lactate dehydrogenase （LDH） and MB isoenzyme of creatine kinase （CK-MB） in the serum, and the levels of reactive oxygen species （ROS）, superoxide dismutase （SOD） and glutathione （GSH） in the lung tissues were measured by automatic biochemical analyzer. ELISA and Western blot were used to detect interleukine-1 beta （IL-1β）, IL-6, IL-18 and tumor necrosis factor-alpha （TNF-α） levels in the serum and lung tissues, respectively. The expression of NLRP3, ASC and caspase-1 at mRNA and protein levels was evaluated by RT-qPCR and Western blot.RESULTS： Compared with control group, the inflammation and alveolar interstitial widening were observed in the lung tissues of model mice, and the CRP, ALT, AST, LDH and CK-MB levels were significantly up-regulated （P〈0.05）. The ROS level was increased, while SOD and GSH levels were significantly decreased （P〈0.05）. The levels of IL-1β, IL-6, IL-18 and TNF-α were markedly up-regulated （P〈0.05）. The protein expression of NLRP3, ASC and caspase-1 was also obviously increased （P〈0.05） in model group. Compared with model group, the symptoms above were significantly relieved in Hyp group, and the effect of high-dose Hyp was more apparent than that of the low-dose one.CONCLUSION： Hyperoside suppresses the injury in MPP mice, which may be related to the inhibition of oxidative stress and NLRP3 inflammasome activation.