Hu Yong-zhen, Wang Dian-hong, Luan Yu, Gong Hai-dong
Department of Neurosurgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhonghua Zhong Liu Za Zhi. 2013 Jan;35(1):11-6. doi: 10.3760/cma.j.issn.0253-3766.2013.01.003.
To investigate the therapeutic mechanism of baicalin on rat brain glioma.
Deep brain glioma models were established by injection of glioma cell line C6 cells into the brain of Wistar rats. The rats at 7 days after modeling were randomly divided into tumor control group (0.9% NaCl solution 30 mg×kg(-1)×d(-1) gavage)and experimental groups. The experimental rats was divided into 3 groups: low dose group (50 mg×kg(-1)×d(-1)), middle dose group (100 mg×kg(-1)×d(-1)) and high dose group (200 mg×kg(-1)×d(-1)), given the baicalin by gavage. Pathological and electron microscopic changes were observed. The expressions of p53 and Bcl-2 were determined by immunohistochemistry, and the changes of MRI, the average survival time and body weight of the rats in each group after treatments were analyzed.
Compared with the control group, the tumor diameter and volume of high dose group rats before sacrifice were significantly reduced (P < 0.01), and the survival time was significantly prolonged (P < 0.01). Immunohistochemistry revealed strong positive expression rate of mutant p53 (84.47 ± 3.74)% and moderately positive rate (47.28 ± 2.38)% in the control group, significantly higher than that in the negative group (12.91 ± 1.07)% (P < 0.01). The positive rate of mutant p53 of the high dose group was (46.42 ± 2.19)%, significantly lower than that of the control group (84.47 ± 3.74)% (P < 0.01). The expression rate of Bcl-2 in the control group was strongly positive (86.51 ± 4.17)% and moderate positive (48.19 ± 2.11)%, significantly higher than that of the negative group (10.36 ± 1.43)% (P < 0.01). Electron microscopy revealed that baicalin caused damages of the cell nuclei and organelles in the gliomas.
Baicalin has significant inhibitory effect on glioma in vivo, and its mechanism may be related to cell apoptosis induced by down-regulated expression of mutant p53, but not related with Bcl-2 expression.
探讨黄芩苷对大鼠脑胶质瘤的治疗机制。
将胶质瘤细胞系C6细胞注入Wistar大鼠脑内建立深部脑胶质瘤模型。造模7天后的大鼠随机分为肿瘤对照组（0.9%氯化钠溶液30mg×kg⁻¹×d⁻¹灌胃）和实验组。实验组大鼠分为3组：低剂量组（50mg×kg⁻¹×d⁻¹）、中剂量组（100mg×kg⁻¹×d⁻¹）和高剂量组（200mg×kg⁻¹×d⁻¹），给予黄芩苷灌胃。观察病理及电镜变化。采用免疫组化法检测p53和Bcl-2的表达，并分析各组大鼠治疗后MRI变化、平均生存时间及体重。
与对照组相比，高剂量组大鼠处死前肿瘤直径和体积明显减小（P<0.01），生存时间明显延长（P<0.01）。免疫组化显示对照组突变型p53强阳性表达率为（84.47±3.74）%，中度阳性率为（47.28±2.38）%，明显高于阴性组（12.91±1.07）%（P<0.01）。高剂量组突变型p53阳性率为（46.42±2.19）%，明显低于对照组（84.47±3.74）%（P<0.01）。对照组Bcl-2表达率强阳性为（86.51±4.17）%，中度阳性为（48.19±2.11）%，明显高于阴性组（10.36±1.43）%（P<0.01）。电镜显示黄芩苷可导致胶质瘤细胞核及细胞器损伤。
黄芩苷对体内胶质瘤有显著抑制作用，其机制可能与下调突变型p53表达诱导细胞凋亡有关，而与Bcl-2表达无关。
