白细胞介素-10对大鼠脊髓损伤后神经细胞凋亡的影响  被引量:3

Effect of Interleukin-10 on rat neurons apoptosis after spinal cord injury

在线阅读下载全文

作  者:彭昊[1] 刘世清[1] 周华[1] 郭卫春[1] 任岳[1] 

机构地区:[1]武汉大学人民医院骨科,430060

出  处:《中华实验外科杂志》2003年第12期1125-1126,共2页Chinese Journal of Experimental Surgery

摘  要:目的 观察白细胞介素-10(IL-10)对大鼠脊髓损伤(SCI)后脊髓细胞凋亡的影响,探讨IL-10对脊髓损伤的保护作用。方法 将SD大鼠随机分为3组:单纯SCI组(A组)、IL-10治疗组(B组)及假损伤组(Sham组)。除Sham组不致伤脊髓外,A、B两组应用改良的Allen打击法制作大鼠急性 SCI模型,B组大鼠于 SCI后 30 min腹腔注射 10 μg IL-10,再分别于伤后 12、24、48 h、4、8、16和 24 d应用苏木素-伊红(HE)染色、原位末端脱氧核糖核苷酸转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记技术(TUNEL检测法)及开放野行为评分(BBB评分)观察IL-10治疗后脊髓细胞凋亡的变化及神经功能的恢复情况。结果 假损伤组未见凋亡细胞。A组大鼠伤后 12 h即可见零星的凋亡细胞,至 24 h渐增多,伤后 48 h脊髓组织凋亡细胞率达峰值。B组伤后 24、48 h及4d细胞凋亡率比单纯SCI组明显减少,差异具有显著性(P<0.01或P<0.05)。B组脊髓功能恢复亦比A组有明显提高(P<0.05)。结论 SCI后早期应用IL-10可抑制大鼠脊髓细胞凋亡,从而对脊髓损伤起到保护作用。Objective To investigate the effect of interleukin-10 (IL-10) on rat neural cell apop- tosis after experimental spinal cord injury (SCI). Methods The experimental rats were divided into three groups: SCI group (group A), IL-10 group (group B) and sham group (no spinal cord injury). The SCI model was induced using the modified Allen technique and the rats in group B were treated with IL- 10 at 30 min after SCI. The apoptosis and functional recovery of the injured spinal cord were evaluated by HE staining, TUNEL method and BBB open-field behavioral test respectively at 12 h, 24 h, 48 h, 4 d, 8 d, 16 d and 24 d after SCI. Results Apoptotic cells were noted primarily at 12 h, and peaked at 48 h af- ter SCI. The apoptotic rate in group B was significantly decreased as compared with that in group A at the time points of 24 h, 48 h, 4 d after SCI (P < 0. 01, or P < 0. 05), and the functional recovery was better in group B than in group A. Conclusion The early adminstration of IL-10 could inhibit apoptosis after SCI.

关 键 词:白细胞介素-10 大鼠 脊髓损伤 神经细胞凋亡 保护作用 

分 类 号:R651.2[医药卫生—外科学] R-33[医药卫生—临床医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象