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目的通过检测全反式维甲酸(ATRA)处理对小鼠短暂性大脑中动脉缺血(tMCAO)后24 h的脑梗死容积以及不同时期脾脏内CD4+CD25+Foxp3+调节性T细胞(Treg)的变化,探讨ATRA是否具有通过干预Treg分化实现对小鼠缺血性脑损伤的保护作用。方法 60只昆明小鼠随机分为预处理组(n=40)和后处理组(n=20)。每组再分为tMCAO联合ATRA处理组,tMCAO联合DMSO对照组。预处理组在小鼠tMCAO前1周开始每天腹腔注射含100 mL/L DMSO的ATRA(10 mg/kg,1次/d)或100 mL/L DMSO(n=20/组)。7 d后处死一部分小鼠行流式细胞术(FCM)测定Treg在脾细胞中的百分率(n=10/组),另一部分小鼠通过腔内线栓法建立tMCAO模型(n=10/组),24 h后进行神经行为学评分(NDS),其后行氯化三苯基四氮唑(TTC)染色观察脑梗死容积。后处理组在小鼠tMCAO模型建立后,即刻腹腔注射ATRA(10 mg/kg)或相等体积的100 mL/L DMSO(n=10/组),24 h后行NDS,测定脑梗死容积和Treg在脾细胞内的百分率。结果 ATRA预处理7 d未能改善小鼠tMCAO后24 h的神经功能障碍(P>0.05),未能降低的脑梗死容积(P>0.05)。ATRA后处理可以明显改善小鼠tMCAO后24 h的神经功能障碍(P<0.05),显著降低脑梗死容积(P<0.05)。然而,ATRA预处理和后处理对小鼠脾脏内的Treg均无影响(P>0.05)。结论在小鼠tMCAO前给予ATRA处理7 d对脑缺血损伤无保护作用,在小鼠tMCAO后及时给予ATRA治疗后24 h有显著的保护作用,但与调节Treg分化无明显关系。
Objective To investigate the effects of all-trans retinoic acid (ATRA) on the volume of cerebral infarction and the percentage of CD4 + CD25 + Foxp3 + regulatory T cells (Tregs) in the spleen after transient traumatic cerebral ischemia (tMCAO) To investigate whether ATRA can protect mice from ischemic brain injury by interfering with Treg differentiation. Methods Sixty Kunming mice were randomly divided into pretreatment group (n = 40) and post-treatment group (n = 20). Each group was further divided into tMCAO combined with ATRA treatment group, tMCAO combined with DMSO control group. The pretreatment group was given intraperitoneal injection of ATRA (10 mg / kg, once a day) or 100 mL / L DMSO (n = 20 / group) containing 100 mL / L DMSO once a week before tMCAO. A portion of mice were sacrificed 7 days later. Flow cytometry (FCM) was used to determine the percentage of Tregs in splenocytes (n = 10 / group). Another group of mice was given tMCAO by endoluminization (n = 10 / group) Neurobehavioral score (NDS) was performed 24 hours later, and the cerebral infarction volume was observed by TTC staining. After the establishment of tMCAO model in mice, intraperitoneal injection of ATRA (10 mg / kg) or an equal volume of 100 mL / L DMSO (n = 10 / group) The percentage within the spleen cells. Results ATRA preconditioning for 7 days did not improve the neurological dysfunction 24 h after tMCAO in mice (P> 0.05), failed to reduce the volume of cerebral infarction (P> 0.05). ATRA postconditioning could significantly improve neurological dysfunction 24 h after tMCAO in mice (P <0.05), and significantly reduce the volume of cerebral infarction (P <0.05). However, ATRA pretreatment and postconditioning had no effect on Treg in spleens of mice (P> 0.05). CONCLUSION: ATRA treatment for 7 days on mice before tMCAO has no protective effect on cerebral ischemic injury, and there is a significant protective effect 24 hours after ATRA treatment in mice immediately after tMCAO, but it has no significant relationship with the regulation of Treg differentiation.