復(fù)方丹參注射液對感染休克大鼠腦損傷時NO、bcl-2及S100B的影響
本文選題:復(fù)方丹參注射液 + NO ; 參考:《南昌大學(xué)》2013年碩士論文
【摘要】:目的:探討復(fù)方丹參注射液對感染性休克大鼠腦損傷時NO、bcl-2及S100B的影響。 方法:選2周齡健康Wistar大鼠40只,隨機分為四個組,每組10只。正常對照組即頸動脈插管監(jiān)測血壓,在其他組給予藥物時給予生理鹽水替代;感染性休克組1(6h)及感染性休克組2(12h)即頸動脈插管監(jiān)測血壓,通過尾靜脈給予脂多糖(5mg/kg)復(fù)制感染性休克模型,血壓降為原來的2/3,伴躁動、皮膚發(fā)紺等現(xiàn)象說明造模成功;復(fù)方丹參注射液治療組即造模成功后通過腹腔注射給予復(fù)方丹參注射(5ml/kg)。除感染性休克組2于造模成功12h取材外,其余三組均于造模后6小時取材,用硝酸還原法檢測四組鼠腦組織中NO的含量,免疫組化法檢測四組鼠海馬組織中bcl-2的表達(dá)及ELISA法檢測四組鼠靜脈血S100B。 結(jié)果: 1.腦組織NO的含量:感染性休克組1(6h)NO含量高于正常組(P0.05),與感染性休克組1相比,治療組NO含量明顯降低(P0.05),但是感染性休克組2(12h)NO含量高于感染性休克組1(6h)(P0.05)。 2.海馬組織bcl-2的表達(dá):正常組、感染性休克組1(6h)及治療組三組組間比較有統(tǒng)計學(xué)差異(P0.05)。與正常組比較,,感染性休克組1及治療組bcl-2的表達(dá)均明顯增多(P0.05),且治療組較感染性休克組1bcl-2表達(dá)增多(P0.05),但是感染性休克組2(12h)bcl-2表達(dá)低于感染性休克組1(6h)(P0.05)。 3.血清S100B的含量:感染性休克組1(6h)S100B含量高于正常組(P0.05),與感染性休克組1相比,治療組S100B含量明顯降低(P0.05),但是感染性休克組2(12h)S100B含量高于感染性休克組1(6h)P0.05)。 4.腦組織病理學(xué)改變:正常對照組:腦組織切片細(xì)胞層次清晰,結(jié)構(gòu)完整,神經(jīng)細(xì)胞胞質(zhì)豐富,核質(zhì)細(xì),核仁清楚;感染性休克組1及感染性休克組2:正常組織結(jié)構(gòu)消失或結(jié)構(gòu)欠清,間質(zhì)水腫,神經(jīng)細(xì)胞排列紊亂,結(jié)構(gòu)模糊,部分細(xì)胞壞死;復(fù)方丹參治療組:正常組織結(jié)構(gòu)尚存在,間質(zhì)水腫輕,神經(jīng)細(xì)胞排列規(guī)則,細(xì)胞核固縮少,結(jié)構(gòu)較完整。 5.腦組織NO含量與海馬組織bcl-2相關(guān)性分析:腦組織NO含量與海馬組織bcl-2之間存在負(fù)相關(guān)(r=-0.928,P 0.05)。 6.腦組織NO含量與血清S100B含量相關(guān)性分析:腦組織NO含量與血清S100B之間存在正相關(guān)(r=0.877,P0.05)。結(jié)論: 1.NO參與了感染性休克腦損傷的過程,可能與其下調(diào)bcl-2有關(guān)。 2.NO和S100B共同參與了感染性休克腦損傷的過程。 3.S100B的表達(dá)可以反映感染性休克時腦損傷的程度。 4.感染性休克時,復(fù)方丹參注射液對腦組織具有保護(hù)作用,可能與抑制NO的生成,上調(diào)bcl-2的表達(dá)有關(guān)。
[Abstract]:Objective: to investigate the effect of compound salvia miltiorrhiza injection on NO-BCL 2 and S 100B during brain injury in rats with septic shock. Methods: 40 2-week healthy Wistar rats were randomly divided into four groups with 10 rats in each group. The blood pressure was monitored by carotid artery intubation in the normal control group, and replaced by normal saline in the other groups; in the septic shock group, the blood pressure was monitored by carotid artery catheterization for 1 to 6 h) and the septic shock group for 21 ~ 12 h), the blood pressure was monitored by carotid artery intubation. The septic shock model was established by injecting lipopolysaccharide (LPS) 5 mg / kg via tail vein. The blood pressure dropped to 2 / 3 of the original, accompanied by restlessness and cyanosis. The treatment group of compound salvia miltiorrhiza injection was given 5 ml / kg of compound salvia miltiorrhiza injection by intraperitoneal injection. Except for the septic shock group (group 2), the other three groups were collected at 6 hours after modeling, and the contents of no in the brain tissue of the four groups were detected by nitric acid reduction method. Immunohistochemical method was used to detect the expression of bcl-2 in hippocampal tissue of the four groups and ELISA method to detect S100B in the venous blood of the four groups. Results: 1. No content in brain tissue: 1(6h)NO content in septic shock group was higher than that in normal group. Compared with septic shock group 1, no content in treatment group was significantly lower than that in septic shock group, but 2(12h)NO content in septic shock group was higher than that in septic shock group at 16 h. 2. The expression of bcl-2 in hippocampal tissue: normal group, septic shock group (1: 6 h) and treatment group (P 0.05). Compared with the normal group, the expression of bcl-2 in the septic shock group and the treatment group was significantly higher than that in the septic shock group, and the expression of 1bcl-2 in the treatment group was higher than that in the septic shock group, but the 2(12h)bcl-2 expression in the septic shock group was lower than that in the septic shock group at 16 h. 3. The content of serum S100B: the content of 1(6h)S100B in septic shock group was higher than that in normal group (P 0.05). Compared with septic shock group 1, the content of S100B in treatment group was significantly lower than that in septic shock group, but the content of 2(12h)S100B in septic shock group was higher than that in septic shock group at 1 h after shock. 4. Brain histopathological changes: normal control group: the level of brain tissue slice cells is clear, the structure is complete, the nerve cell cytoplasm is abundant, the nucleus is fine, the nucleolus is clear; Septic shock group 1 and septic shock group 2: normal tissue structure disappeared or not clear, interstitial edema, nerve cell arrangement disorder, fuzzy structure, partial cell necrosis, compound salvia miltiorrhiza treatment group: normal tissue structure still existed, The interstitial edema is light, the nerve cells are arranged regularly, the nucleus is less pyknosis and the structure is relatively complete. 5. The correlation between no content in brain tissue and bcl-2 in hippocampus: there was a negative correlation between no content and bcl-2 in hippocampus (P 0.05). 6. The correlation between no content in brain tissue and serum S100B content: there was a positive correlation between no content in brain tissue and serum S100B content. Conclusion: 1.NO is involved in the process of septic shock brain injury and may be related to its down-regulation of bcl-2. 2.NO and S100B are involved in the process of septic shock brain injury. The expression of 3.S100B can reflect the degree of brain injury in septic shock. 4. In septic shock, compound salvia miltiorrhiza injection has protective effect on brain tissue, which may be related to inhibition of no production and up-regulation of bcl-2 expression.
【學(xué)位授予單位】:南昌大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2013
【分類號】:R459.7
【參考文獻(xiàn)】
相關(guān)期刊論文 前10條
1 韓若東;湯其強;肖晗;李俊;;丹參酮ⅡA對早期腦缺血和腦缺血再灌注損傷的腦保護(hù)作用[J];安徽醫(yī)科大學(xué)學(xué)報;2012年06期
2 白慧健;邢開宇;石靜;;家兔急性腦干機械性損傷后星形膠質(zhì)細(xì)胞S100β表達(dá)與損傷時間的關(guān)系[J];實用醫(yī)學(xué)雜志;2012年05期
3 張紅燕;;膿毒癥腦病的研究進(jìn)展[J];醫(yī)學(xué)理論與實踐;2012年03期
4 吳儉;萬芳;汪翠婷;袁高樂;;丹參對感染性休克大鼠腦組織保護(hù)作用的實驗研究[J];南昌大學(xué)學(xué)報(醫(yī)學(xué)版);2011年09期
5 潘翠改;李家瓊;許鐵;李茂琴;;感染性休克時線粒體損傷機制的研究進(jìn)展[J];中華臨床醫(yī)師雜志(電子版);2011年18期
6 張芳艷;梅崢嶸;陳少銳;劉培慶;;隱丹參酮對谷氨酸誘導(dǎo)的皮層神經(jīng)元凋亡的保護(hù)作用[J];重慶醫(yī)科大學(xué)學(xué)報;2011年06期
7 萬芳;吳儉;汪翠婷;袁高樂;;重組人促紅細(xì)胞生成素對感染性休克大鼠腦組織的保護(hù)作用[J];南昌大學(xué)學(xué)報(醫(yī)學(xué)版);2011年03期
8 支文煜;;腦缺血再灌注損傷引起的線粒體功能障礙及丹參酮ⅡA的保護(hù)作用研究[J];實用心腦肺血管病雜志;2010年10期
9 閆菊;;氧自由基及其清除劑對新生兒缺氧缺血性腦病的作用[J];醫(yī)學(xué)信息(中旬刊);2010年07期
10 林翔;張俐;劉蔚楠;聶光瑞;伏勇;曾啟清;;丹參酮對脊髓缺血再灌注損傷大鼠模型脊髓、血清谷氨酸含量的影響[J];海峽藥學(xué);2010年05期
相關(guān)碩士學(xué)位論文 前1條
1 張穎;丹酚酸B對腦缺血小鼠腦組織線粒體作用及其機制的研究[D];北京中醫(yī)藥大學(xué);2007年
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