自己找一些资料来看的,并作翻译。文章如下:
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.
对啮齿动物的大量研究表明,姜黄素在众多慢性疾病的动物模型中有抗炎症、抗增生和抗氧化等作用,提示姜黄素是一个多效性分子。
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].
目前研究发现,姜黄素可预防神经退行性、心血管、肺、代谢性等方面疾病以及肿瘤,如其能开启囊性纤维化跨膜转运调节体通道,进而调整囊性纤维化。
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) 主动脉缩窄and phenylephrin infusion脱氧肾上腺素, echocardiographic parameters
超声心动图参数 and gene expression of hypertrophic markers.
另外,姜黄素还能通过抑制p300组蛋白乙酰基转移酶(p300-HAT)活性来预防心肌肥大和心力衰竭。Li等(年份)研究表明,姜黄素可防治小鼠由主动脉缩窄、脱氧肾上腺素灌注、超声心动图参数和肥大性基因表达标记导致的心肌肥大。
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.
这种效应的实现是通过:1)抑制组蛋白乙酰化修饰、GATA结合蛋白-4乙酰化和DNA结合的过程,而这个过程与p300组蛋白乙酰基转移酶活性有关;2)破坏依赖p300组蛋白乙酰基转移酶的信号途径,阻止主动脉缩窄导致的炎症发生和纤维化。这提示,姜黄素可通过抑制p300组蛋白乙酰基转移酶活,从而被认为是防治心肌肥大、炎症发生和纤维化的潜在药物。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)对两种不同心力衰竭模型的体内研究表明也发现了类似结果,患有高血压性心脏病盐敏感性Dahl大鼠和和手术性导致的心肌梗塞的大鼠,其收缩性功能退化和心理衰竭,导致心肌厚度和直径增加,而姜黄素防止了这一过程。另外该研究还报道,姜黄素抑制p300-HAT活性,为人类治疗心力衰竭提供了一种新的思路。
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.
大量研究还表明,姜黄素在许多代谢性疾病也发挥着作用,如其能改善II-糖尿病的症状。肥胖是II-糖尿病发生的一种重要诱因,而II-糖尿病特点是有炎性成份的产生及其病理症状。Weisberg等(年份)通过对葡萄糖胰岛素耐受性和血红素Alc的分析结果表明,姜黄素可改善高脂肪导致肥胖和leptin缺失ob/ob雄性C57BL/6J小鼠的糖尿病症状,显著降低巨噬细胞对白色脂肪组织的浸润,增加脂肪组织脂联素的产生,降低肝组织细胞因子NF-kB活性,减轻肝肿大和肝标记炎症,显示口服姜黄素可治疗炎症和与肥胖相关的代谢紊乱,改善II型糖尿病小鼠降血糖的机制。
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.
研究报道,姜黄素可通过抑制NF-kB依赖基因的表达,预防酒精导致大鼠肝疾病的发生。饲喂鱼油+酒精的日粮,试验大鼠发生脂肪肝、肝坏死和炎症,并伴随NFkB活化和致使细胞因子、趋化因子、COX-2、可诱导性一氧化氮合成酶以及硝基酪氨酸的产生。用姜黄素处理可防止酒精介导肝脏病理、生理生化的变化。内毒素对Kupffer细胞的毒害作用是酒精肝的一个特点,而姜黄素能抑制内毒素对分离Kupffer细胞(枯否细胞)作用。由此看来,姜黄素通过抑制内毒素介导的NF-kB活化作用和Kupffer细胞中依赖NF-kB的基因表达,如细胞因子、趋化因子、COX-2和一氧化氮合成酶的基因表达,从而阻止试验模型酒精肝发生。
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,研究报道姜黄素可调节生物标记化合物,进而改善酒精性和非酒精性的胰腺炎。类似于一些致肿瘤坏死因子阻滞剂如humira、remicade、enbrel等一样,姜黄素在Crohn疾病、牛皮癣和风湿性疾病同样有治疗价值。通过抑制体内淀粉样boligomers、原纤维和结合斑块的产生,显示姜黄素在Alzheimer病中有治疗效果。研究证实,先天免疫在Alzheimer病发生过程中具有重要的作用,而姜黄素具有免疫调节作用(38,39)。姜黄素能下调MMP-9和MMP-2的表达,阻止吲哚美辛导致胃溃疡的发生。 |