曲尼斯特滴眼液在兔眼小梁切除术后应用的免疫组化研究

目的通过单克隆抗增殖细胞核抗原抗体（PCNA）和TGF—β1免疫组化的研究，评估曲尼斯特在兔眼实验性小梁切除术后抗纤维化方面的作用。方法27只兔子（54眼）随机分为对照组、MMC组、曲尼斯特组；双眼均行标准小梁切除术。MMC组术中应用丝裂霉素C（MMC）．曲尼斯特组术后应用曲尼斯特滴眼液。术后7天、14天、28天各组处死兔子3只，眼球组织固定，PCNA和TGF—β1免疫组化染色并进行PCNA计数和计算TGF—β1染色平均光密度。结果术后7天、14天对照组PCNA阳性细胞明显多于MMC组和曲尼斯特组（P〈0．05），而曲尼斯特组和MMC组相比差异无统计学意义（P〉0．05）。曲尼斯特组TGF—β1的平均光密度值明显小于对照组，差异具有统计学意义俨〈0．05），而与MMC组比较差异无统计学意义（P〉0．05）。结论曲尼斯特应用于青光眼滤过术后能抑制成纤维细胞增殖，其作用机制可能是通过直接抑制成纤维细胞增殖及减少TGF—β1分泌而间接抑制其增殖。

Immunohistochemistry study of Tranilast eye drops applied in rabbits after glaucoma filtering surgery

OBJECTIVE Through PCNA and TGF-β1 immunohistochemistry staining on iiltering blebs after applications of tranilast postoperatively to explore its role and mechanism of anti-scar effect after filtering surgery. METHODS Twenty-seven rabbits （54 eyes） were divided into three groups： control group, MMC-treated group and tranilast-treated group respectively. Trabeculectomy was performed on each eye. In MMC treated group, 0.4 mg/ml MMC were used during operation and, 0.5% tranilast eyedrops were used after operation in tranilast treated group. Three rabbits of each group were killed randomly on postoperative day 7, 14 and 28 respectively. Proliferation of fibroblast were observed by immunohistochemistry staining of proliferative cell nuclear antigen （PCNA） and TGF-β1 on conjunctiva and sclera of filtering area of the rabbits. RESULTS There were more PCNA positive cells in control group than the other two groups on postoperative day 7, 14 （P〈0.05）. There were no differences between MMC treated group and tranilast treated group （P〉0.05）. The positive area of TGF-β1 and average optical density in control group were smaller than that in other two groups （P〈0.05） and no significant difference was observed between the MMC-treated group and tranilast-treated group （P〉0.05）. CONCLUSIONS Tranilast can inhibit the proliferation of fibroblast in glaueoma filtering surgery. The mechanism of the effect includes the direct antiproliferation of fibroblast and indirect action through inhibit secretion of TGF-β1.