中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2010年
10期
863-865
,共3页
薛晶%付铁娟%李丽%戈亚萍%冯加纯
薛晶%付鐵娟%李麗%戈亞萍%馮加純
설정%부철연%리려%과아평%풍가순
脑缺血%再灌注损伤%炎性介导素类%细胞凋亡%蛋白酶抑制药
腦缺血%再灌註損傷%炎性介導素類%細胞凋亡%蛋白酶抑製藥
뇌결혈%재관주손상%염성개도소류%세포조망%단백매억제약
Brain ischemia%Reperfusion injury%Inflammation mediators%Apoptosis%Protease inhibitors
目的 观察硼替佐米对脑缺血再灌注后炎性反应及细胞凋亡的影响,探讨其脑保护作用机制.方法 将15只大鼠随机分为假手术组、生理盐水组、硼替佐米组各5只.脑缺血2 h再灌注即刻给予硼替佐米0.2 mg/kg尾静脉注射,对照组以等量生理盐水尾静脉注射,再灌注后24 b取材.免疫组化法测组织核因子(NF)-κBp65、白细胞介素(IL)-1β;缺口末端标记法检测神经细胞凋亡.结果假手术组偶见NF-κBp65、IL-1β免疫反应阳性细胞[分别为(1.21±0.16)个/400倍、(11.56±0.99)个/400倍],凋亡细胞亦少见[(2.88±0.27)个/400倍],生理盐水组与硼替佐米组均可见大量NF-κBp65、IL-1β免疫反应阳性细胞及凋亡细胞[分别为(56.28±1.95)个/400倍与(29.76±2.53)个/400倍、(47.64±2.06)个/400倍与(29.6±1.61)个/400倍、(51.05±4.23)个/400倍与(33.44±2.06)个/400倍],差异有统计学意义(均P＜0.05).结论 蛋白酶体抑制剂硼替佐米可通过减少NF-κB的激活,抑制炎性反应,减少细胞凋亡,对缺血脑组织有保护作用.
目的 觀察硼替佐米對腦缺血再灌註後炎性反應及細胞凋亡的影響,探討其腦保護作用機製.方法 將15隻大鼠隨機分為假手術組、生理鹽水組、硼替佐米組各5隻.腦缺血2 h再灌註即刻給予硼替佐米0.2 mg/kg尾靜脈註射,對照組以等量生理鹽水尾靜脈註射,再灌註後24 b取材.免疫組化法測組織覈因子(NF)-κBp65、白細胞介素(IL)-1β;缺口末耑標記法檢測神經細胞凋亡.結果假手術組偶見NF-κBp65、IL-1β免疫反應暘性細胞[分彆為(1.21±0.16)箇/400倍、(11.56±0.99)箇/400倍],凋亡細胞亦少見[(2.88±0.27)箇/400倍],生理鹽水組與硼替佐米組均可見大量NF-κBp65、IL-1β免疫反應暘性細胞及凋亡細胞[分彆為(56.28±1.95)箇/400倍與(29.76±2.53)箇/400倍、(47.64±2.06)箇/400倍與(29.6±1.61)箇/400倍、(51.05±4.23)箇/400倍與(33.44±2.06)箇/400倍],差異有統計學意義(均P＜0.05).結論 蛋白酶體抑製劑硼替佐米可通過減少NF-κB的激活,抑製炎性反應,減少細胞凋亡,對缺血腦組織有保護作用.
목적 관찰붕체좌미대뇌결혈재관주후염성반응급세포조망적영향,탐토기뇌보호작용궤제.방법 장15지대서수궤분위가수술조、생리염수조、붕체좌미조각5지.뇌결혈2 h재관주즉각급여붕체좌미0.2 mg/kg미정맥주사,대조조이등량생리염수미정맥주사,재관주후24 b취재.면역조화법측조직핵인자(NF)-κBp65、백세포개소(IL)-1β;결구말단표기법검측신경세포조망.결과가수술조우견NF-κBp65、IL-1β면역반응양성세포[분별위(1.21±0.16)개/400배、(11.56±0.99)개/400배],조망세포역소견[(2.88±0.27)개/400배],생리염수조여붕체좌미조균가견대량NF-κBp65、IL-1β면역반응양성세포급조망세포[분별위(56.28±1.95)개/400배여(29.76±2.53)개/400배、(47.64±2.06)개/400배여(29.6±1.61)개/400배、(51.05±4.23)개/400배여(33.44±2.06)개/400배],차이유통계학의의(균P＜0.05).결론 단백매체억제제붕체좌미가통과감소NF-κB적격활,억제염성반응,감소세포조망,대결혈뇌조직유보호작용.
Objective To observe the effects of velcade on inflammatory reaction and cell apoptosis after ischemia-reperfusion injury, and to explore the neuroprotective mechanism of velcade.Methods The 15 male Wistar rats were randomly divided into sham-operated group, physiological saline control group and velcade-treated group (n= 5, each). The model of temporary middle cerebral artery occlusion (MCAO) was applied and reperfused after 2 hours. Immediately after the reperfusion, all rats were performed intraperitoneal injection with velcade 0. 2 mg/kg in velcadetreated group, and with the same volume of physiological saline in control group. After 24 hours, the rats were decapitated in all groups. The apoptosis cells were found by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and the expressions of nuclear factor-κBp65 (NF-κBp65) and interleukinh-1β (IL-1β) were detected by immunohistochemistry. Results The immunologically positive cells of NF-κBp65, IL-1β and apoptosis cells were occasionally found in shamoperated group [(1.21 ± 0. 16)/400 power, (11.56 ± 0. 99)/400 power and (2. 88 ± 0. 27)/400 power], while a lot of immunologically positive cells of NF-κBp65, IL-1β and apoptosis cells were found in velcade-treated group and control group. The control with compared group, these cells were significantly more in the velcade-treated group [(56.28± 1.95)/400 power vs. (29. 76±2.53)/400 power, (47. 64±2.06)/400 power vs. (29.6±1. 61)/400 power and (51. 05±4. 23)/400 power vs.(33.44±2.06)/400 power, all P＜0. 05]. Conclusions The velcade could decrease the expressions of the NF-κBp65 and IL-1β and diminish the neuronal apoptosis. The neuroprotective mechanism of velcade may lie in decreasing apoptosis through inhibiting inflammation.
