16,16二甲基前列腺素E_2对博莱霉素致大鼠肺纤维化的干预作用

Investigation of the Role of Prostaglandin E_2 in Pulmonary Fibrosis Induced by Bloemycin Treatment

目的 :探讨 1 6 ,1 6二甲基前列腺素E2 (dmPGE2 )在博莱霉素诱导大鼠肺纤维化进程中对结缔组织生长因子 (CTGF)表达水平的影响。方法 :通过苏木素伊红 (HE)染色及Ⅰ型胶原 (Col Ⅰ )、Ⅲ型胶原 (Col Ⅲ )免疫组化染色评价纤维化程度 ,用原位杂交方法检测结缔组织生长因子 (CTGF)的mRNA在肺内的表达情况 ,用免疫组化法检测转化生长因子 β1 (TGF β1 )及cAMP依赖性磷脂酶A(PKA)的表达。结果 :①模型组中TGF β1 、CTGFmR NA、Col Ⅰ、Col Ⅲ表达水平较空白组明显增高 ;②实验组中CTGFmRNA和Col Ⅰ、Col Ⅲ水平与模型组比明显下降 ,较正常组稍高。结论 :PGE2 可减轻博莱霉素所诱导的肺间质纤维化程度 。

Objective: To study the role of exogenic dmPGE 2 in progresse of pulmonary fibrosis in rats. Methods: 63 Wistar rats were divided into three groups: the normal control group ,the model group treated with bleomycin and the dmPGE 2 group which were given dmPGE 2 1nmol·kg -1 ·d -1 intraperitoeally after given bleomycin as model group. All rats were sacrificed on day 7,14,28 after treatment respectively. Immunohistochemical evaluation was used to detect the expression of TGF β 1, collagenⅠand collagenⅢ protein. In situ hybridization method was used to observe the expression level of connective tissue growth factor (CTGF) mRNA. Results: ① The levels of the expression of CTGF mRNA and TGF β 1 were significantly increased in the model group. ② In the dmPGE 2 group,the levels of CTGF mRNA and collagenⅠ, collagenⅢ protein decreased remarkly compared with those in model group. Conclusion: dmPGE 2 may alleviate pulmonarry fibrosis induced by in rats through in inhibiting the expression of CTGF mRNA.