青刺果黄酮对糖尿病大鼠肾组织c-fos基因表达上调的抑制作用

目的探讨青刺果黄酮对糖尿病大鼠肾组织c-fos及c-jun基因表达的影响。方法大鼠随机分为正常对照组（A组）、糖尿病组（B组）及青刺果黄酮治疗组（C组）,采用腹腔单剂量注射链脲佐菌素65mg·kg^-1建立糖尿病大鼠模型。治疗组给予青刺果黄酮300mg·kg^-1·d^-1腹腔注射。分别于第2周和4周末各组随机抽取4只大鼠处死,取肾脏称重;取第4周5只大鼠部分右肾皮质,采用RT-PCR及免疫组织化学方法检测青刺果黄酮对糖尿病大鼠肾组织c-foszaBNA、c-junmRNA及其蛋白表达．的影响。结果糖尿病大鼠肾脏指数显著增加,治疗组肾脏指数显著降低;糖尿病大鼠肾组织c-fosmRNA、c-junmRNA及其蛋白表达明显上调,青刺果黄酮可显著抑制上述指标的表达。结论青刺果黄酮通过抑制糖尿病大鼠肾组织c-fos及c-jun基因表达上调而减轻糖尿病大鼠肾脏损伤。     

液相色谱与质谱联用分析蕲艾总黄酮提取物初步研究

目的：鉴定蕲艾中黄酮类化合物的种类与结构。方法：通过有机溶剂及超声波辅助法提取蕲艾中的有效成份黄酮类化合物,并进行萃取蒸馏,获得溶液中的溶质部分（黄酮类化合物部分）,用高效液相色谱分析其黄酮成分,再通过液相色谱与质谱联用（LC-MS）进行鉴定。结果：从高效液相色谱（HPLC）可分离出20个较好的峰。结论：至少有20种不同结构的黄酮化合物。LC-MS结果表明可能含有32种不同黄酮化合物,从整体上可把握艾叶中黄酮化合物的种类和相对含量。     

含黄酮类中药的抗癌抗肿瘤作用研究概况

黄酮类化合物是自然界中广泛存在的一大类化合物,具有多种多样的生物学活性,其抗癌抗肿瘤作用是目前的研究热点,它在中草药中的分布,引来国内外学者对中草药中黄酮类成分的研究兴趣,发现其抗癌抗肿瘤作用与抗氧化、抗自由基、抑制癌细胞生长、抗致癌因子、调节免疫等作用相关。中草药中白花蛇舌草、陈皮、黄芩、夏枯草、半枝莲等含有较高的黄酮类成分,本文将对中草药中黄酮类成分的抗癌抗肿瘤作用进行介绍。     

血府逐瘀汤联合西药对结核性胸膜炎肺功能及外周血细胞的影响

目的：通过检测胃溃疡寒证模型大鼠体内能量代谢、物质代谢、脂代谢相关酶的含量,考察高良姜、大高良姜、红豆蔻的黄酮类成分对其表达的影响,以阐述其寒热属性及对胃溃疡寒证模型大鼠能量代谢的影响及作用机制。方法：采用知母水煎液和15%冰乙酸灌胃造胃溃疡寒证模型。以干姜姜辣素为阳性对照,分为空白对照组、阳性对照组、模型组、高良姜高低剂量组、大高良姜高低剂量组、红豆蔻高低剂量组,给药2 d,留取血清、肝组织、胃组织,观察大鼠胃组织病理学变化,通过测定Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶水平考察其黄酮类成分对胃溃疡寒证模型大鼠能量代谢的影响,测定琥珀酸脱氢酶（SDH）、肝糖原水平考察对物质代谢的影响,测定游离脂肪酸（FFA）、脂蛋白脂酶（LIPD）、肝脂酶（LIPC）水平考察对脂代谢的影响。同时测定血清中超氧化物歧化酶（SOD）、丙二醛（MDA）水平。结果：与空白对照组比较,模型组大鼠肝组织中Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶、SDH,以及FFA、LIPD、LIPC、SOD水平显著降低（P<0.05,P<0.01）,肝糖原水平和血清中MDA水平显著升高（P<0.05,P<0.01）;与模型组比较,给药组能显著升高肝组织中Ca2+-Mg2+-ATP酶及血清中FFA、SDH水平（P<0.05,P<0.01）;除大高良姜低剂量组、红豆蔻低剂量组外,其余给药组能显著升高肝组织中Na+-K+-ATP酶（P<0.05,P<0.01）;除大高良姜高低剂量组、红豆蔻低剂量组外,其余给药组能显著升高血清SOD水平(P<0.05,P<0.01);除高良姜低剂量组、大高良姜低剂量组外,其余给药组能显著升高LIPD、LIPC水平（P<0.05,P<0.01）;给药组能显著降低肝糖原水平,以及血清MDA水平（P<0.05,P<0.01）。结论：3味山姜属中药黄酮类成分能够促进能量代谢、物质代谢、脂代谢,可初步判断3味山姜属中药黄酮类成分温热属性,也说明其可调节胃溃疡寒证大鼠能量代谢和物质代谢、脂代谢紊乱,同时通过增强抗氧化能力而发挥抗溃疡作用。     

核桃楸皮总黄酮含量测定

目的：测定核桃楸皮总黄酮含量。方法：以芦丁为标准品,紫外分光光度法在410nm测定总黄酮含量。结果：核桃楸皮中总黄酮含量为2.20%。结论：方法灵敏度高,结果可靠。     

一年生黄芩总黄酮含量的动态变化研究

目的：分析一年生黄芩在生殖生长期间，不同部位黄酮含量的动态变化，探讨黄芩的生长特性，为黄芩规范化栽培及开发利用提供依据。方法：应用分光光度法测定不同发育阶段黄芩不同部位总黄酮含量。结果：黄芩不同时期各部位总黄酮含量由高到低的排列顺序是：繁殖部位〉根〉叶〉茎。结论：繁殖部位不同器官总黄酮含量变化趋势基本一致；叶状苞片总黄酮的含量高于叶的含量；茎和花枝总黄酮的含量变化趋势基本一致。     

菝葜中黄酮和芪类成分的研究

目的：为阐明百合科植物菝葜的有效成分，对其根茎进行了化学成分研究。方法：运用层析手段和波谱方法分离并鉴定了5个酚性化合物。结果：它们的结构为二氢山奈酚(dihydrokaempferol,1)，3，5，4′—三羟基芪(3，5，4′-trihydroxystilbene,2)，3，5，2′，4′—四羟基芪(3，5，2′，4′-tetrahydroxystilbene,3)，二氢山奈酚3—O-α—L—鼠李糖等(黄杞苷，dihydrokaempferol 3-O-α-L-rhamnoside,engletin,4)，槲皮素4′—0-β—D—葡萄糖等(quercetin4′—O-β—D—glucoside,5)。结论：5个化合物均为首次从菝葜中得到，其中化合物1，4，5为首次从菝葜属植物中得到。     

Dietary flavonoids protect human colonocyte DNA from oxidative attack in vitro

Summary Background & Aims: Epidemiological studies suggest that antioxidant polyphenols in the human diet may protect against diseases such as cancer. In this study we investigated the cytoprotective potential of the flavonoids, quercetin, myricetin, kaempferol and rutin against oxidative DNA damage in human colonocytes in vitro. Methods: Caco-2 cells, which display specialised enterocyte/colonocyte cell functions, were used as an in vitro model for human colonocytes. Hydrogen peroxide was employed as the oxidant. DNA damage (strand breakage, oxidised purines and oxidised pyrimidines) was determined using the alkaline single cell gel electrophoresis or comet assay. Cell growth and viability were measured. Results: Hydrogen peroxide caused a dose-dependent increase in DNA strand breakage in human colonocytes, presumably via oxygen free radical generation. Quercetin and myricetin protected Caco-2 cells against oxidative attack. In addition, quercetin decreased hydrogen peroxide-mediated inhibition of growth. Neither rutin nor kaempferol was effective. However, quercetin, while inhibiting DNA strand breakage, did not alter the levels of oxidised bases following peroxide treatment. The antifungal agent ketoconazole, prevented quercetin cytoprotection in Caco-2 cells, indicating that P450-mediated metabolism may alter the efficacy of the flavonoids against oxidative DNA damage. Conclusion: Flavonoids, particularly quercetin, the most abundant flavonoid in the human diet, are likely to be important in defending human colonocytes from oxidative attack. Received: 7 October 1998, Accepted: 5 November 1998     

Morin alleviates fructose-induced metabolic syndrome in rats via ameliorating oxidative stress,inflammatory and fibrotic markers

Metabolic syndrome (MBS) is a widespread disease that has strongly related to unhealthy diet and low physical activity, which initiate more serious conditions such as obesity, cardiovascular diseases and type 2 diabetes mellitus. This study aimed to examine the therapeutic effects of morin, as one of the flavonoids constituents, which widely exists in many herbs and fruits, against some metabolic and hepatic manifestations observed in MBS rats and the feasible related mechanisms. MBS was induced in rats by high fructose diet feeding for 12 weeks. Morin (30 mg/kg) was administered orally to both normal and MBS rats for 4 weeks. Liver tissues were used for determination of liver index, hepatic expression of glucose transporter 2 (GLUT2) as well as both inflammatory and fibrotic markers. The fat/muscle ratio, metabolic parameters, systolic blood pressure, and oxidative stress markers were also determined. Our data confirmed that the administration of morin in fructose diet rats significantly reduced the elevated systolic blood pressure. The altered levels of metabolic parameters such as blood glucose, serum insulin, serum lipid profile, and oxidative stress markers were also reversed approximately to the normal values. In addition, morin treatment decreased liver index, serum liver enzyme activities, and fat/muscle ratio. Furthermore, morin relatively up-regulated GLUT2 expression, however, down-regulated NF-κB, TNF-α, and TGF-β expressions in the hepatic tissues. Here, we revealed that morin has an exquisite effect against metabolic disorders in the experimental model through, at least in part, antioxidant, anti-inflammatory, and anti-fibrotic mechanisms.