槲皮素通过PGC-1α通路对创伤性脑损伤的脑保护作用

    Protective Effect of Quercetin on Traumatic Brain Injury Through PGC-1α Signal Pathway

    • 摘要: 目的 研究槲皮素通过PGC-1α通路对创伤性脑损伤(traumatic brain injury,TBI)后神经细胞凋亡的影响。方法 选取48只ICR小鼠,随机分为4组,每组12只:假手术组,TBI组,TBI+溶剂组和TBI+槲皮素组。建立小鼠自由落体撞击脑损伤模型,TBI后30 min给予腹腔注射槲皮素。TBI 24 h后检测小鼠神经学功能评分和脑水肿情况;采用尼氏染色检测TBI后神经细胞凋亡情况; Western blotting检测小鼠神经细胞内外的PGC-1α及Bax、Bcl-2等凋亡相关蛋白的表达情况;采用免疫组化法进一步验证TBI后神经细胞PGC-1α的表达情况。结果 与假手术组相比,TBI组脑水肿与神经细胞凋亡明显增加(P < 0.01); PGC-1α与Bax表达明显增加,而Bcl-2表达明显减少(P < 0.01)。与TBI+溶剂组相比,TBI+槲皮素组脑水肿及神经凋亡明显减轻(P < 0.05),Bax表达明显减少,PGC-1α和Bcl-2表达明显增加(P < 0.05)。结论 槲皮素可通过激活PGC-1α途径减轻TBI后神经细胞凋亡,起到有效的脑保护作用。

       

      Abstract: OBJECTIVE To explore the effect of quercetin on nerve cell apoptosis after traumatic brain injury(TBI) via PGC-1α signal pathway. METHODS Forty eight ICR mice were selected and randomly divided into four groups(n=12 in each group):sham operation group, TBI group, TBI+vehicle group and TBI+quercetin group. Mice model of free falling body impingement brain injury was established and quercetin was injected intraperitoneally 30 min after TBI. Brain edema and neurobehavioral assessments were detected 24 h after TBI. Nissl staining was used for obtain nerve cell apoptosis. The expression of PGC-1α, the level of Bax and Bcl-2 were detected by Western blotting analysis and immumohistochemical staining was used to verify the expression of nerve cell PGC-1α after TBI. RESULTS Compared with sham operation group, brain edema and nerve cell apoptosis of TBI group were increased significantly(P < 0.01). Expression of PGC-1α and Bax were increased significantly, and expression of Bcl-2 decreased(P < 0.01). Compared with TBI + vehicle group, brain edema and nerve cell apoptosis of TBI + quercetin group were decreased significantly(P < 0.05), expression of Bax were decreased significantly, and PGC-1α and Bcl-2 increased significantly(P < 0.05). CONCLUSION Quercetin can reduce the apoptosis of nerve cells after TBI by activating PGC-1α pathway and play an effective role in brain protection.

       

    /

    返回文章
    返回