目的 構(gòu)建慢性阻塞性肺疾?。–OPD）大鼠模型，探討虎杖苷對COPD大鼠PI3K/AKT/mTOR通路以及氣道炎癥的影響。方法 100只Wistar大鼠隨機(jī)分為對照組、模型組、地塞米松（0.2 mg/kg，陽性藥）組和虎杖苷低、高劑量（30、60 mg/kg）組，每組20只。除對照組外，其他組熏香煙加氣管注射內(nèi)毒素法制備COPD模型，COPD造模前1 d開始ig給藥，每天1次，持續(xù)30 d。ELISA法檢測支氣管肺泡灌洗液（BALF）中腫瘤壞死因子（TNF）-α和白細(xì)胞介素（IL）-6水平；RSE3020肺功能檢測儀測定用力肺活量（FVC）、第1秒用力呼氣容積（FEV₁）、呼氣峰流速（PEF）；取肺組織4%甲醛固定后制作切片，HE染色，并進(jìn)行肺組織損傷病理評分；Western blotting檢測肺組織PI3K、AKT、mTOR蛋白表達(dá)。結(jié)果 虎杖苷高、低劑量組大鼠BALF中TNF-α和IL-6表達(dá)水平、肺組織損傷病理評分以及PI3K、AKT和mTOR蛋白表達(dá)均顯著低于模型組（P<0.01）；虎杖苷高、低劑量組大鼠FVC、FEV1、PEF肺功能指標(biāo)顯著高于模型組（P<0.01）。結(jié)論 虎杖苷可以抑制COPD大鼠PI3K/AKT/mTOR通路，抑制氣道炎癥，發(fā)揮肺損傷保護(hù)作用。

Objective To observe the effects of polydatin on PI3K/AKT/mTOR pathway and airway inflammation in rats with chronic obstructive pulmonary disease (COPD). Methods Totally 100 Wistar rats were devided into control group, model group, dexamethasone (0.2 mg/kg, positive drug) group and low and high dose of polydatin (30, 60 mg/kg) groups, with 20 rats in each group. Except for control group, the COPD models were prepared bypassive cigarette smoking and intratracheal. Ig administration was started one day before COPD modeling, once a day, lasting for 30 days. The expression of TNF-α and IL-6 in BALF was detected by ELISA analysis. The FVC, FEV₁, and PEF was used to determined lung function. HE staining was used to determined pathological score of lung tissue injury (LDPS scores). Western blot was used to detect protein expression of PI3K, AKT and mTOR in lung tissue. Results The expression of TNF-α and IL-6 in BALF, LDPS scores, expression of PI3K, AKT, mTOR in low and high dose of polydatin group was significantly lower than that in COPD model group (P<0.01) and the FVC, FEV1, and PEF was significantly higher than that in COPD model group (P<0.01). Conclusion Polydatin can inhibit PI3K/AKT/mTOR pathway to block airway inflammation in rats and protect lung destroy in COPD rats.

R285.5

海南省自然科學(xué)基金面上項(xiàng)目（818MS136）