淫羊藿苷对大鼠创伤性脑损伤后白细胞介素1β和肿瘤坏死因子α的作用

Effects of icariin on IL-1β and TNF-α after traumatic brain injury in rats

目的观察淫羊藿苷(Ica)对大鼠创伤性脑损伤(TBI)后炎症因子白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的影响。方法 SD雄性大鼠60只,随机分为空白组、模型组、Ica低剂量(10 mg·kg^(-1))组和Ica高剂量(40 mg·kg-1)组,均n=15。造模前一周连续预防性灌胃给药,每日2次,空白组和模型组灌胃给予等体积生理盐水。采用Feeney法建立大鼠TBI模型,造模24 h后取材,取材前先进行神经行为学功能评分;HE染色法观察脑组织病理形态学变化;Real-Time PCR法检测损伤区皮质中IL-1β和TNF-αm RNA的表达;免疫组化法观察损伤区皮质中IL-1β和TNF-α表达情况;Western blot检测损伤区皮质中IL-1β和TNF-α蛋白表达。结果与空白组相比,模型组大鼠神经行为学功能评分明显升高(P<0.01),损伤区能观察到明显的病理学损伤,损伤区皮质中IL-1β和TNF-αm RNA和蛋白的表达均明显上调(P<0.05或P<0.01)。与模型组相比,Ica低、高剂量组大鼠神经行为学功能评分显著降低(P<0.01),且损伤区组织的病理学损伤减轻;Ica低剂量组损伤区皮质中IL-1β和TNF-αm RNA表达显著下调(P<0.05),但Ica高剂量组TNF-αm RNA表达无显著改变(P>0.05);Ica低、高剂量组IL-1β和TNF-α蛋白的表达均显著下调(P<0.05或P<0.01)。结论 Ica对TBI具有改善作用,其中一个重要的原因可能与抑制炎症因子IL-1β、TNF-α的表达有关。

AIM To observe the influence of icariin （Ica） on inflammatory eytolcines IL- 1β and TNF-α which is caused by traumatic brain injury （TBI）. METHODS Sixty SD male rats were randomly divided into control group, model group, lea low dose group （10 mg·kg-1） and high dose group （40 mg·kg-1）, with 15 rats in each group. The rats were treated with Ica or normal saline twice a day for one week before TBI. Rats were sacrificed 24 hours after TBI model was made by Freeney method. Neuroethology function of rats was evaluated. Pathology change of brain tissue was observed by HE staining. The mRNA expression of IL- 1β and TNF-α in the injured brain cortex were detected by RT-PCR. And the protein expression of IL-1β and TNF-α in the injured brain cortex were detected by immunohistoehemistry and Western blot. RESULTS Compared with the control group, the neuroethology evaluation points of rats in the model group increased significantly （P 〈 0.01 ） , and the pathology damage of injured tissue were observed clearly in the injured cortex, in which the expression of IL- 1β and TNF-α protein and mRNA increased obviously （P 〈 0.05 or P 〈 0.01 ）. Compared with the model group, the neuroethology evaluation points of rats decreased significantly in the Ica low and high groups （P 〈 0.01） , and the pathology damage of injured tissue also reduced. The expression of IL-1β and TNF-α mRNA decreased significantly in the lea low group （P 〈 0.05 or P 〈 0.01 ）. However, there was no significant difference in mRNA expression of TNF-α in the Ica high group （P 〉 0.05）. The expression of IL-1β and TNF-α protein in both groups decreased significantly （P 〈 0.05 or P 〈 0.01）. CONCLUSION Ica could improve the TBI, which may be associated with the inhibition of inflammatory eytokines IL-1 β and TNF-α expression.