Pharmacological effects in animals
Numerous studies carried out in rodents show that curcumin is active in numerous animal models for chronic diseases(Figure 3). The anti-inflammatory, antiproliferative and antioxidant effects of curcumin described earlier indicate that curcumin is a highly pleiotropic molecule.
對嚙齒動物的大量研究表明，姜黃素在眾多慢性疾病的動物模型中有抗炎癥、抗增生和抗氧化等作用，提示姜黃素是一個多效性分子。
This phytochemical has now been found to prevent neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases [29]. For instance, curcumin was found to correct cystic fibrosis through opening of the cystic fibrosis transmembrane-conductance-regulator channels [30].
Curcumin was also found to prevent cardiac hypertrophy and heart failure through the inhibition of p300 histone acetyltransferase (HAT) [31,32]. Li et al. [31] showed that this phytochemical can both prevent and reverse mouse cardiac hypertrophy induced by aortic banding (AB) 主動脈縮窄and phenylephrin infusion脫氧腎上腺素, echocardiographic parameters
超聲心動圖參數(shù) and gene expression of hypertrophic markers.
另外，姜黃素還能通過抑制p300組蛋白乙酰基轉移酶（p300-HAT）活性來預防心肌肥大和心力衰竭。Li等（年份）研究表明，姜黃素可防治小鼠由主動脈縮窄、脫氧腎上腺素灌注、超聲心動圖參數(shù)和肥大性基因表達標記導致的心肌肥大。
This effect correlated with inhibition of histone acetylation, GATA binding protein (GATA)-4 acetylation and DNA binding, all through inhibition of p300-HAT activity. Curcumin also blocked AB-induced inflammation and fibrosis through disrupting p300-HAT-dependent signaling pathways. These results, thus, indicate that curcumin has the potential to protect against cardiac hypertrophy, inflammation and fibrosis through suppression of p300-HAT activity.
這種效應的實現(xiàn)是通過：1）抑制組蛋白乙酰化修飾、GATA結合蛋白-4乙?；虳NA結合的過程，而這個過程與p300組蛋白乙?；D移酶活性有關；2）破壞依賴p300組蛋白乙?；D移酶的信號途徑，阻止主動脈縮窄導致的炎癥發(fā)生和纖維化。這提示，姜黃素可通過抑制p300組蛋白乙酰基轉移酶活，從而被認為是防治心肌肥大、炎癥發(fā)生和纖維化的潛在藥物。Similarly, Morimoto et al. [32] examined the effects of curcumin in vivo in two different heart failure models: hypertensive heart disease in saltsensitive Dahl rats and surgically induced myocardial infarction in rats. In both models, curcumin prevented deterioration of systolic function and heart-failure-induced increases in both myocardial-wall thickness and diameter[31]. They also indicated that inhibition of p300-HAT activity by curcumin provides a novel therapeutic strategy for heart failure in humans.
Morimoto等（年份）對兩種不同心力衰竭模型的體內研究表明也發(fā)現(xiàn)了類似結果，患有高血壓性心臟病鹽敏感性Dahl大鼠和和手術性導致的心肌梗塞的大鼠，其收縮性功能退化和心理衰竭，導致心肌厚度和直徑增加，而姜黃素防止了這一過程。另外該研究還報道，姜黃素抑制p300-HAT活性，為人類治療心力衰竭提供了一種新的思路。
Curcumin has also been found to affect various metabolic diseases. Numerous studies indicate that this polyphenol can improve the symptoms associated with type 2 diabetes. Obesity is a major risk factor for the development of type 2 diabetes, and both conditions are now recognized to possess substantial inflammatory components underlying their pathophysiologies. As determined by glucoseand insulin-tolerance testing and hemoglobin A1c, Weisberg et al. [33] reported that curcumin can ameliorate diabetes in high-fat diet-induced obese and leptin-deficient ob/ob male C57BL/6J mice. They showed that curcumin treatment also significantly reduced macrophage infiltration of white adipose tissue, increased adipose tissue adiponectin production and decreased hepatic NF-kB activity, hepatomegaly and markers of hepatic inflammation. This data shows that orally ingested curcumin can reverse the inflammatory and metabolic derangements associated with obesity and improves glycemic control in mouse models of type 2 diabetes.
Another study reported that curcumin can prevent alcohol-induced liver disease (ALD) in rats by inhibiting the expression of NF-kB-dependent genes [34]. Rats fed fish oil plus ethanol developed fatty liver, necrosis and inflammation, which was accompanied by activation of NFkB and the induction of cytokine, chemokine, COX-2, inducible nitric oxide synthase (iNOS) and nitrotyrosine formation. Curcumin treatment prevented both the pathological and biochemical changes induced by alcohol. Curcumin also suppressed the stimulatory effects of endotoxin in isolated Kupffer cells, which is implicated in the pathogenesis of ALD. This agent inhibited endotoxin-mediated activation of NF-kB and suppressed the expression of cytokines, chemokines, COX-2 and iNOS in Kupffer cells. Thus, curcumin prevents experimental ALD, in part by suppressing induction of NF-kB-dependent genes.
研究報道，姜黃素可通過抑制NF-kB依賴基因的表達，預防酒精導致大鼠肝疾病的發(fā)生。飼喂魚油+酒精的日糧，試驗大鼠發(fā)生脂肪肝、肝壞死和炎癥，并伴隨NFkB活化和致使細胞因子、趨化因子、COX-2、可誘導性一氧化氮合成酶以及硝基酪氨酸的產(chǎn)生。用姜黃素處理可防止酒精介導肝臟病理、生理生化的變化。內毒素對Kupffer細胞的毒害作用是酒精肝的一個特點，而姜黃素能抑制內毒素對分離Kupffer細胞（枯否細胞）作用。由此看來，姜黃素通過抑制內毒素介導的NF-kB活化作用和Kupffer細胞中依賴NF-kB的基因表達，如細胞因子、趨化因子、COX-2和一氧化氮合成酶的基因表達，從而阻止試驗模型酒精肝發(fā)生。
Additionally, curcumin has been reported to ameliorate both ethanol- and non-ethanol-induced experimental pancreatitis through the modulation of biomarkers as indicated earlier [35]. Like TNF inhibitors (e.g. humira, remicade and enbrel), curcumin also has potential therapeutic value against Crohn’s disease, psoriasis and rheumatic diseases [36]. This yellow chemical also exhibits activity against Alzheimer’s diseases (AD) as indicated by its ability to inhibit the formation of amyloid b oligomers and fibrils, bind plaques and reduce amyloid in vivo [37]. Innate immunity also has an important role in the activity of curcumin against AD [38]. Immunomodulatory effects of curcumin are also well documented [39]. Indomethacininduced gastric ulcer is prevented by curcumin through the downregulation of MMP-9 and MMP-2 [40].
此外，研究報道姜黃素可調節(jié)生物標記化合物，進而改善酒精性和非酒精性的胰腺炎。類似于一些致腫瘤壞死因子阻滯劑如humira、remicade、enbrel等一樣，姜黃素在Crohn疾病、牛皮癬和風濕性疾病同樣有治療價值。通過抑制體內淀粉樣boligomers、原纖維和結合斑塊的產(chǎn)生，顯示姜黃素在Alzheimer病中有治療效果。研究證實，先天免疫在Alzheimer病發(fā)生過程中具有重要的作用，而姜黃素具有免疫調節(jié)作用（38，39）。姜黃素能下調MMP-9和MMP-2的表達，阻止吲哚美辛導致胃潰瘍的發(fā)生。作者: leijian 時間: 2009-1-9 17:30
關于姜黃素的文章一大把，主要作用有抗氧化（是否能改善肉質呢？）、抗菌(包括細菌和真菌，是否有替代抗生素，促進動物生長作用呢？)、調控機體代謝作用（是否可改善動物生長呢？）等等。有條件的朋友可以嘗試啊。作者: leijian 時間: 2009-1-9 17:34 本帖最后由 leijian 于 2009-1-9 17:36 編輯