本文選題：咖啡因 + 肝纖維化�。� 參考：《中南大學(xué)》2014年碩士論文

【摘要】：目的：利用咖啡因干預(yù)四氯化碳(Carbon tetrachloride, CCl4)誘導(dǎo)SD大鼠所形成的肝纖維化,并觀察大鼠相關(guān)指標(biāo)的變化,并探討咖啡因可能的治療機(jī)制。 方法：把SD大鼠100只隨機(jī)分為4組,每組25只,并予橄欖油3ml/(kg大鼠體重)皮下注射空白對(duì)照組(n=25),每周2次,共注射8周；將含50%CC14的橄欖油混合溶液以3ml/(kg大鼠體重)皮下注射于模型組(n=25)及咖啡因治療組(n=25)予以,每周2次,共注射8周；咖啡因?qū)φ战M(n=25)不予以肝纖維化造模處理。同時(shí),咖啡因治療組和咖啡因?qū)φ战M均于第一周開(kāi)始予以咖啡因灌胃,50mg/(kg大鼠體重),1次/日；以羧甲基纖維素鈉(Sodium carboxymethyl cellulose, CMC-Na)用于空白對(duì)照組和模型組的大鼠進(jìn)行灌胃治療,方法同咖啡因,共治療8周。在第九周時(shí),大鼠被麻醉后將其處死并稱(chēng)量,分別取肝臟相同部位組織分別進(jìn)行HE染色和Masson染色并進(jìn)行評(píng)分,取其肝組織進(jìn)行HE、Masson染色,進(jìn)行肝臟炎癥活動(dòng)度半定量評(píng)分和肝組織纖維化半定量評(píng)分,采用免疫組織化學(xué)染色后檢測(cè)肝組織α-平滑肌肌動(dòng)蛋白(Alpha-Smooth muscle actin, α-SMA)的表達(dá)量,并采用實(shí)時(shí)熒光定量聚合酶鏈反應(yīng)(Real time quantitative Polymerase Chain Reaction, Real time qPCR)檢測(cè)轉(zhuǎn)化生長(zhǎng)因子-β1(Transforming growth factor-beta1, TGF-β1)、結(jié)締組織生長(zhǎng)因子(Connective tissue growth factor, CTGF)和α-SMA的表達(dá)量。 結(jié)果：與空白對(duì)照組相比較,大鼠(模型組)的體重變化、病理評(píng)分、TGF-β1、CTGF和α-SMA的表達(dá)有明顯的增高(P0.01)；與模型組相比較,大鼠(咖啡因治療組)體重變化、肝纖維化病理評(píng)分、TGF-β1、CTGF的表達(dá)有明顯的下降(p0.01),而α-SMA的表達(dá)與TGF-β1、CTGF的表達(dá)相比較,前者的降低程度相對(duì)不明顯(p0.05),但是仍然具有統(tǒng)計(jì)學(xué)意義；將咖啡因?qū)φ战M與空白對(duì)照組進(jìn)行比對(duì)時(shí),上述檢測(cè)數(shù)據(jù)均無(wú)明顯統(tǒng)計(jì)學(xué)差異,即p0.05。 結(jié)論：(1)咖啡因能在一定程度上抑制由CC14誘導(dǎo)的SD大鼠所形成的實(shí)驗(yàn)性肝纖維化；(2)在短期內(nèi)(8周)持續(xù)攝入咖啡因后,健康大鼠的肝臟未見(jiàn)顯著性改變(P0.05)；(3)咖啡因的抗肝纖維化機(jī)制可能為：抑制肝臟炎癥反應(yīng),抑制HSCs及MFs的活化(a-SMA表達(dá)下調(diào)),減少促肝纖維化因子如TGF-β1和CTGF的表達(dá),導(dǎo)致ECM的合成與降解失衡,從而抑制肝纖維化。
[Abstract]:Aim: to investigate the effects of caffeine on hepatic fibrosis induced by carbon tetrachloride (CCL 4) in SD rats, and to investigate the possible therapeutic mechanism of caffeine. Methods: 100 SD rats were randomly divided into 4 groups, 25 rats in each group, and subcutaneously injected with olive oil 3ml/ (kg rat body weight) as control group (n = 25), twice a week for 8 weeks. Olive oil containing 5014 was subcutaneously injected into the model group (n = 25) and caffeine treatment group (n ~ (25) twice a week for 8 weeks with 3ml/ (kg body weight), while the control group (n ~ (25) was not treated with liver fibrosis. At the same time, caffeine treatment group and caffeine control group were given caffeine 50 mg / (kg body weight) once a day at the beginning of the first week, and sodium carboxymethyl cellulosein (CMC-Na) was used to treat rats in blank control group and model group. Methods caffeine was used for 8 weeks. At the ninth week, the rats were killed and weighed after anesthesia. The liver tissues were stained with HE and Masson respectively, and the liver tissues were stained with HE and Masson. The expression of alpha-Smooth muscle actin (偽 -SMA) in liver tissue was detected by immunohistochemical staining. Real time quantitative polymerase chain reaction (Real time qPCR) was used to detect the expression of transforming growth factor-beta 1 (TGF- 尾 1), connective tissue growth factor, growth factor (CTGF) and 偽 -SMA. Results: compared with the control group, the expression of TGF- 尾 1 CTGF and 偽 -SMA in the model group was significantly higher than that in the control group (P0.01), and the weight of the rats in the caffeine treatment group was significantly higher than that in the caffeine treatment group (P0.01), and the expression of TGF- 尾 1 CTGF and 偽 -SMA in the model group was significantly higher than that in the control group (P0.01). The expression of TGF- 尾 1 CTGF in hepatic fibrosis was significantly decreased (p0.01), while the expression of 偽 -SMA was not significantly decreased (p0.05), but still statistically significant, compared with that of TGF- 尾 1, the caffeine control group was compared with the blank control group. There was no significant difference in the above data, namely, p0.05. Conclusion: (1) caffeine can inhibit experimental hepatic fibrosis induced by CC14 in SD rats to a certain extent, (2) there is no significant change in liver of healthy rats after continuous caffeine intake for 8 weeks (P0.05). (3) the anti-hepatic fibrosis mechanism of caffeine may be as follows: inhibiting hepatic inflammation, inhibiting the activation of HSCs and MFs (down regulation of a-SMA expression), reducing the expression of hepatic fibrosis promoting factors such as TGF- 尾 1 and CTGF, leading to the imbalance of synthesis and degradation of ECM, thus inhibiting hepatic fibrosis.
【學(xué)位授予單位】：中南大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類(lèi)號(hào)】：R575.2

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本文編號(hào)：2069336