目的 考察注射用丹參多酚酸（SAFI）對腦缺血再灌注大鼠腦損傷的保護(hù)作用。方法 線拴法構(gòu)建大腦中動脈缺血再灌注（MCAO/R）大鼠模型，將造模成功的大鼠隨機(jī)分為模型組、丁苯酞氯化鈉注射液（陽性藥，9 mL·kg^-1）組和SAFI低、中、高劑量（5.85、11.71、23.42 mg·kg^-1，11.71 mg·kg^-1為臨床等效劑量）組，每組12只。假手術(shù)組和模型組給予0.9%氯化鈉注射液，SAFI每天給藥1次，丁苯酞氯化鈉注射液每天給藥2次，尾iv連續(xù)給藥14 d。給藥期間稱大鼠體質(zhì)量；給藥前后對各組大鼠進(jìn)行神經(jīng)功能評分；給藥后采用TTC染色法檢測腦梗死體積；酶聯(lián)免疫吸附（ELISA）法檢測血清中γ干擾素（IFN-γ）、白細(xì)胞介素-6（IL-6）、白細(xì)胞介素-1β（IL-1β）、腫瘤壞死因子-α（TNF-α）和超氧化物歧化酶（SOD）的水平；HE染色觀察腦組織病理形態(tài)；尼氏染色觀察海馬區(qū)尼氏小體形態(tài)變化情況。結(jié)果 給藥14 d后，與模型組比較，SAFI 5.85、11.71、23.42 mg · kg^-1組和丁苯酞氯化鈉注射液組大鼠體質(zhì)量顯著增加（P ＜ 0.001），腦組織梗死體積顯著縮小（P＜0.001） ；SAFI 11.71、23.42 mg·kg^-1組和丁苯酞氯化鈉注射液組神經(jīng)功能評分顯著降低（P＜0.05、0.01），IFN-γ、IL-1β和TNF-α水平均顯著降低（P＜0.01、0.001），SOD水平顯著升高（P＜0.01、0.001）； SAFI 23.42 mg·kg^-1組和丁苯酞氯化鈉注射液組IL-6水平顯著降低（P＜0.05、0.01）； SAFI可明顯改善MCAO/R大鼠腦組織缺血半暗帶區(qū)病理損傷，抑制尼氏小體數(shù)的減少。結(jié)論 SAFI對腦缺血再灌注大鼠腦損傷具有明顯的保護(hù)作用。

Objective To investigate the protective effect of Salvianolic Acid for Injection (SAFI) on brain injury after cerebral ischemia reperfusion in rats. Methods The rat model of middle cerebral artery ischemia reperfusion (MCAO/R) was established by the method of tethering. The rats with successful modeling were randomly divided into model group, Butylphthalide Sodium Chloride Injection (BSCI, positive drug, 9 mL·kg^-1) group and SAFI low, medium and high dose (5.85, 11.71, 23.42 mg·kg^-1, 11.71 mg·kg^-1 was the clinical equivalent dose) group, with 12 rats in each group. The sham-operation group and model group were given 0.9% sodium chloride injection, the SAFI group was given once a day, and the BSCI was given twice a day, and the tail iv was given continuously for 14 days. Weigh the weight of rats during administration. After 14 days, the changes of neurological function scores before and after administration were compared. The volume of cerebral infarction was detected by TTC staining. The contents of interferon- γ (IFN- γ), interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor- α (TNF- α) and superoxide dismutase (SOD) in serum were detected by enzyme-linked immunosorbent assay. HE staining was used to observe the pathological morphology of brain tissue. Morphological changes of Nissl bodies in hippocampus were observed by Nissl staining. Results After 14 days of administration, compared with model group, the body mass of rats in SAFI 5.85, 11.71, 23.42 mg·kg^-1 group and BSCI group increased significantly (P< 0.001), and the infarct volume of brain tissue decreased significantly (P< 0.001). Compared with model group, SAFI 11.71, 23.42 mg·kg^-1 group and BSCI group had significantly lower neurological function scores (P< 0.05, 0.01), the level of SOD in serum was significantly increased, and the levels of INF-γ, IL-1β, IL-6 and TNF-ɑ were decreased (P< 0.01, 0.001). The level of IL-6 in SAFI 23.42 mg·kg^-1 group and BSCI group decreased significantly compared with model group (P< 0.05, 0.01). SAFI could significantly improve the pathological damage of ischemic penumbra in MCAO/R rats and inhibit the reduction of Nissl corpuscles compared with model group. Conclusion SAFI has a significant protective effect on brain injury of cerebral ischemia-reperfusion rats.

R285.5