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目的研究重组人生长激素(recombinant human growth hormone,rhGH)对烟雾吸入性损伤大鼠肺泡Ⅱ型细胞(ATⅡ)增殖及Bcl-2和Bax蛋白表达的影响。方法清洁级雄性SD大鼠70只,体重160~180g,采用随机数字表法随机分为3组:正常对照组(C组)、单纯吸入性损伤组(I组)和吸入性损伤+rhGH治疗(R组),后2组各再分为6、10、14日亚组。烟雾造成吸入性肺损伤模型,rhGH经腹部皮下注入(1.33U/kg),连续应用7d。各时相点剖胸取肺,行常规病理切片进行病理形态学观察并用免疫组化方法观察肺泡Ⅱ型细胞(ATⅡ)增殖以及Bcl-2和Bax蛋白表达的变化。结果rhGH能显著增加新增殖ATⅡ数量;正常大鼠肺组织Bcl-2和Bax mRNA无表达,皮下注射rhGH后6、10、14日R组Bcl-2蛋白表达阳性细胞分别为(31.01±2.70)、(52.34±3.44)、(50.15±4.00)个/HP,明显高于Ⅰ组的(24.76±2.82)、(37.92±4.28)、(35.58±3.64)个/HP(P<0.05);R组Bax蛋白表达阳性细胞为(21.16±2.79)、(31.22±5.62)、(26.27±5.41)个/HP,明显低于Ⅰ组[(26.51±2.61)、(41.50±4.14)、(34.55±2.94)个/HP,P<0.05]。结论经皮下注入外源性rhGH能有效刺激ATⅡ的增殖,上调Bcl-2蛋白表达及下调Bax蛋白表达,改变Bcl-2/Bax的比值从而抑制细胞凋亡。
Objective To investigate the effects of recombinant human growth hormone (rhGH) on proliferation and expression of Bcl-2 and Bax protein in alveolar type Ⅱ cells (AT Ⅱ) induced by smoke inhalation injury in rats. Methods Seventy male Sprague Dawley rats weighing 160 ~ 180g were randomly divided into three groups: normal control group (C group), simple inhalation injury group (I group) and inhalation injury + rhGH treatment (R group). The latter 2 groups were subdivided into subgroups of 6,10 and 14 days. Inhalation of lung injury caused by smoke model, rhGH subcutaneous injection (1.33U / kg), continuous application of 7d. Pulmonary dissection was performed at all time points. Pathological examination was performed by routine pathological sections. The proliferation and expression of Bcl-2 and Bax in alveolar type Ⅱ cells (AT Ⅱ) were observed by immunohistochemistry. Results rhGH significantly increased the number of newly proliferating ATⅡ. The expression of Bcl-2 and Bax mRNA in the lung tissue of normal rats was not detected. The number of Bcl-2 positive cells in R group after subcutaneous injection of rhGH for 6, 10 and 14 days were (31.01 ± 2.70) , (52.34 ± 3.44) and (50.15 ± 4.00) / HP, respectively, which were significantly higher than those in group Ⅰ (24.76 ± 2.82), (37.92 ± 4.28) and (35.58 ± 3.64) /HP (21.16 ± 2.79), (31.22 ± 5.62) and (26.27 ± 5.41) / HP in B group were significantly lower than those in B group [(26.51 ± 2.61), (41.50 ± 4.14), (34.55 ± 2.94) /HP,P<0.05]. Conclusions Exogenous rhGH can effectively stimulate the proliferation of AT Ⅱ, up-regulate the expression of Bcl-2 and down-regulate the expression of Bax, and change the ratio of Bcl-2 / Bax to inhibit apoptosis.