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目的探讨乌司他丁对大鼠视网膜紫外线光损伤的保护作用及其机制。方法将36只SD大鼠随机分为对照组、光损伤组和给药组,每组各12只计24只眼。采用光照强度为(2 200±138)Lux的300~400 nm紫外线间歇照射法制作视网膜损伤模型。光照前3 d起,给药组腹腔单剂量注射乌司他丁2×104U·kg-1·d-1,其他组给予等量生理盐水腹腔注射至取标本日。分别于光损伤后3 d、7 d处死大鼠,摘出眼球。HE染色后观察大鼠视网膜的组织学变化,免疫组织化学方法检测B细胞淋巴瘤/白血病-2蛋白(Bcl-2)和Bcl-2相关X蛋白(Bax)在视网膜的相对表达量。结果对照组大鼠视网膜结构完整,层次清楚;光损伤组的视网膜结构紊乱,且随时间延长紊乱程度明显加重;给药组大鼠视网膜形态较对照组稍微紊乱,但紊乱程度均轻于相同时间段光损伤组。光损伤组大鼠的视网膜外核层(outer nuclear layer,ONL)厚度均低于同时间段对照组(P<0.05,P<0.01);给药组大鼠的各时间段视网膜ONL厚度均高于同时间段光损伤组(P<0.05,P<0.01),但低于正常对照组(P均<0.01)。光损伤组中Bax蛋白在视网膜的相对表达量明显高于对照组,给药组中,Bax在视网膜的表达也较对照组明显增强,但明显弱于相应时间段光损伤组(P均<0.05)。光损伤组的Bcl-2蛋白在视网膜的相对表达量明显低于对照组(P<0.05),给药组Bcl-2蛋白相对表达量较对照组明显降低(P<0.05),但较相应时间段光损伤组的相对表达量明显增加(P<0.05)。结论乌司他丁对紫外线照射造成的视网膜损伤具有保护作用,其机制可能与乌司他丁抑制Bax蛋白表达而促进Bcl-2蛋白表达从而抑制紫外线诱导的凋亡有关。
Objective To investigate the protective effect of ulinastatin on the retinal damage induced by ultraviolet light in rats and its mechanism. Methods Thirty-six Sprague-Dawley rats were randomly divided into control group, light injury group and administration group, 12 eyes in each group, 24 eyes. The retinal damage model was made by intermittent UV irradiation at 300-400 nm with a light intensity of (2 200 ± 138) Lux. The rats in the treatment group received intraperitoneal injection of ulinastatin 2 × 104 U · kg-1 · d-1 for 3 d before light irradiation, and the other groups were injected intraperitoneally with the same amount of saline until the day of taking the sample. Rats were sacrificed 3 days and 7 days after light injury, respectively, and their eyes were excised. The histological changes of the retina were observed by HE staining. The relative expression of Bcl-2 and Bax in the retina was detected by immunohistochemistry. Results The retinal structure of the rats in the control group was intact and the level was clear. The retina structure in the light injury group was disordered and the disturbance of the retina was obviously aggravated with time. The morphology of retina in the treated group was slightly disordered compared with that of the control group, but the degree of disorder was lighter than the same time Light damage group. The thickness of the outer nuclear layer (ONL) in the light-injured group was lower than that in the control group at the same time (P <0.05, P <0.01). The ONL thickness of the retina in each group was significantly higher (P <0.05, P <0.01), but lower than the normal control group (P <0.01). The relative expression of Bax protein in retina in photodamaged group was significantly higher than that in control group. The expression of Bax in retina of photodamage group was significantly higher than that in control group, but was weaker than that in photodamage group (P <0.05) ). Compared with the control group, the relative expression of Bcl-2 protein in the light-injured group was significantly lower than that in the control group (P <0.05), and the relative expression of Bcl-2 protein in the injured group was significantly lower than that in the control group The relative expression of light injury group increased significantly (P <0.05). Conclusion Ulinastatin can protect against retinal damage caused by ultraviolet radiation. The possible mechanism is that Ulinastatin can inhibit the expression of Bax protein and promote the expression of Bcl-2 protein so as to inhibit UV-induced apoptosis.