Ultraviolet radiation-induced lipid peroxidation in liposomal membrane: Modification by capsaicin

Ultraviolet-radiation has been reported to cause lipid peroxidation in the liposomal membrane. In the present study, treatment with capsaicin, (8-methyl-n-vanillyl-6-nonenamide), the pungent principle of red hot pepper, was shown to modify UV-induced lipid peroxidation in the liposomal membrane. Treatment with low doses of capsaicin (less than 0.1 μg/mL of phosphatidyl choline liposome) produced a significant increase in UV-induced lipid peroxidation, while high doses (0.1–0.5 μg/mL of PC liposome) caused a significant decrease of UV-induced peroxidation. These pro-oxidant and antioxidant activities of capsaicin over UV-induced liposomal lipid peroxidation were also comparable to experiments modulated with standard pro-oxidant ferrous sulphate and antioxidant sodium azide. The observed dual nature of capsaisin's action on the UV-induced lipid peroxidation of the liposomal membrane may be attributed to the previously reported “activation” followed by “desensitization” action of capsaicin on other membrane lipid systems.     

Histomorphological and biochemical changes of lung tissues following capsaicin treatment in the rat

Gross histomorphological alterations and biochemical changes, particularly in the lipid pattern of lung alveolar tissues, were oblerved in rats after intraperitoneal injection of capsaicin (the pungent principle of red hot pepper). Preliminary experiments showed that short-term capsaicin treatment produced and inflammatory response with significant degenerative changes in the alveolar epithelial cells and increased cellularity of lung alveoli, as revealed by thickening of lung alveolar cells with occasional rupture of lung alveolar cellular integrity. The cytological changes were correlated with concomitant biochemical changes revealed by the decreased cholesterol and phospholipid content of lung alveolar tissues and infiltration of phospholipids towards the lumen of the alveoli which may be the cause of thickening of the alveoli cell lining of the lung tissues. On the other hand, long term capsaicin-treated rat lungs showed a significant inhibition of capsaicin induced damage of lung tissues indicating a possible dual action of capsaicin on antiinflammatory respones in the pulmonary system.     

Effects of short-term capsaicin treatment on formalin and nitrogen dioxide induced changes in lipid peroxidation and antioxidant enzyme system in rat lung

Exposure of rats to formalin and nitrogen dioxide vapour caused a significant increase in values of the lung wet wt/dry wt ratio (oedema formation) and lipid peroxidation. These effects were not observed in rats treated with short-term capsaicin, either before or after exposure to the two gases. This protective action of short-term capsaicin treatment can possibly be linked with the strengthening of the pulmonary antioxidant enzyme defence system by capsaicin.     

Protection of lipid peroxidation and carbonyl formation in proteins by capsaicin in human erythrocytes subjected to oxidative stress

Capsaicin (8-methyl-N-vanillyl-6-nonemide) is the major pungent principle found in hot peppers of the plant genus Capsicum. The present work was undertaken to investigate the antioxidative property of capsaicin on markers of oxidative stress; membrane lipid peroxidation (formation of malondialdehyde) and membrane carbonyl groups in human erythrocytes. The effect of capsaicin has been compared with l-ascorbic acid. Subjecting erythrocytes to oxidative stress by incubating them with t-BHP caused a significant increase in MDA level and protein carbonyl group content above the basal value. The presence of capsaicin (10 microm) in the incubation medium protected the erythrocytes from t-BHP-induced oxidative stress as evidenced by the decrease in MDA level and protein carbonyl group content, l-ascorbic acid also showed similar protective effect. The results conclusively prove the efficacy of the antioxidant property of capsaicin. This evidence suggests that dietary factors that act as antioxidants to decrease membrane lipid peroxidation and protein carbonyl formation may contribute to a protective effect against cancer, atherosclerosis and age related diseases. This antioxidant effect may, in part, explain the high consumption of capsicum in certain regions of the world.     

Capsaicin action modulates lipid peroxidation induced by different irritants

Capsaicin (8-methyl-n-vanillyl-6-nonenamide), the pungent principle of red hot pepper, has been reported to cause ‘activation’ followed by ‘desensitization’ of the tissue against various types of irritant induced damage, on short- and long-term application respectively. This review discusses one aspect of the mechanism of capsaicin induced activation followed by desensitization by discussing the modulatory effects of capsaicin on lipid peroxidative changes caused by different irritants (e.g. gaseous, chemical and radiation).     

虫草多糖对二甲基亚硝胺诱导的肝纤维化大鼠脂质过氧化及肝细胞再生的影响

目的:观察虫草多糖对二甲基亚硝胺(DMN)诱导的大鼠肝纤维化的药理作用.方法:采用DMN大鼠肝纤维化模型,分为正常组(N,n=6)、模型组(M,n=11)、虫草多糖组(C,n=8)、秋水仙碱组(Q,n=9).造模4周,虫草多糖(60 mg·kg-1)和秋水仙碱(0.1 mg·kg-1)灌胃给药3周,模型与正常组国时给予等量灭菌水.观察血清ALT,AST,GGT活性及Alb,TBil含量;肝组织羟脯氨酸(Hyp)含量;肝脏病理及胶原染色;肝组织SOD活性及MDA,GSH,GSH-Px含量;肝脏组织增殖细胞核抗原(PCNA)蛋白表达.结果:模型组血清ALT,AST,GGT,TBil显著升高,Alb显著降低,虫草多糖组血清AST,TBil显著降低,Alb显著升高;模型组肝组织Hyp显著升高,虫草多糖、秋水仙碱组则显著降低;HE染色:模型组正常肝小叶结构破坏,肝细胞水肿,汇管区结缔组织增生,虫草多糖及秋水仙碱组上述病理变化显著减轻.胶原染色:模型组肝小叶纤维间隔形成,见较多完整假小叶;虫草多糖、秋水仙碱组胶原沉积减少.模型组肝组织SOD,GSH-Px,GSH显著降低,MDA显著增高,虫草多糖及秋水仙碱组GSH,GSH-Px活性显著增高.模型组肝组织PCNA蛋白表达显著升高,虫草多糖及秋水仙碱组则显著降低.结论:虫草多糖可显著抑制DMN诱导的大鼠肝纤维化及脂质过氧化损伤.     

氯乙醇引起大鼠肝线粒体钙泵的抑制途径的初步探讨

 目的：探讨氯乙醇（CE）对肝线粒体钙泵的影响及其钙泵抑制的机制。方法：CE与肝线粒体共同温浴，分别测定丙二醛（MDA）、蛋白巯基及钙泵的变化。结果：CE能引起线粒体的脂质过氧化（LPO），表现为MDA升高，同时，还引起蛋白巯基的降低和钙泵的抑制，与对照组比较具有显著性意义，且存在着剂量 反应关系及时间 反应关系。在本实验条件下，发现CE引起的蛋白巯基的降低与钙泵抑制呈平衡关系。用巯基供剂二硫苏糖醇（DTT）能部分地拮抗CE引起肝线粒体LPO，保护了线粒体蛋白巯基，从而保护了钙泵。结论：钙泵的抑制可能与LPO耗竭蛋白巯基有关。     

Capsaicin pretreatment protects free radical induced rat lung damage on exposure to gaseous chemical lung irritants

Pretreatment with capsaicin tends to normalize pulmonary lipid peroxidation changes induced by exposure to sulfur dioxide, formalin or nitrogen dioxide gases. This protective effect of capsaicin pretreatment appears to be due to the stabilization of the rat lung membrane lipid system.     

姜黄素抗大鼠肝星状细胞氧应激脂质过氧化作用的研究

目的:探讨姜黄素(Curcumin,Cur)对大鼠肝星状细胞(hepatic stellate cells,HSC)氧应激所致脂质过氧化的作用.方法:HSC与FeNTA共同培养产生氧应激.以MTT法检测姜黄素对HSC增殖的效应,LDH法检测姜黄素对HSC的毒性作用,以ELISA法测定细胞培养液中Ⅰ型胶原的水平,以试剂盒分别测定细胞培养液中MDA、GSH、GSH-PX、SOD水平.结果:HSC与FeNTA共同培养,细胞内MDA、GSH水平明显升高,GSH-PX、SOD活力明显降低.FeNTA与HSC共同培养,能明显促进HSC增殖和提高细胞培养上清中Ⅰ型胶原的水平.姜黄素可以逆转上述所有FeNTA所致效应.结论:姜黄素抗肝纤维化作用可能与其抗脂质过氧化作用有关.     

Studies on the effects of capsaicin on leakage in egg lecithin (Phosphatidyl Choline) liposome membranes in vitro

Capsaicin (8-methyl-n-vanillyl-6-nonenamide), caused a concentration dependent leakage of chromate through an egg lecithin (phosphatidyl choline) liposomal preparation. Capsaicin treatment of liposomal suspensions caused a maximum leakage of marker chromate at 20 min and then attained a plateau from 30 min onward. Treatment of liposomes with various concentrations of capsaicin (μg/mL loposomal suspensions) showed that lower concentrations of capsaicin (< 0-0.1 μg/mL) caused greater chromate leakage than higher concentrations (0.1-0.5 μg/mL). This dual effect of capsaicin on liposome membrane was accompanied by an increased amount of malondialdehyde formed (an important end product of lipid peroxidation) at lower concentrations (<0.10 μg/mL) than at higher concentrations (0.1-0.5 μg/mL).     

Effects of black tea extract on carbon tetrachloride-induced lipid peroxidation in liver, kidneys, and testes of rats

Previous studies have shown that green tea and black tea have antioxidant effects and chemopreventive activity against chronic disease including some forms of cancer. We have, therefore, examined the effects of an aqueous extract of black tea against carbon tetrachloride-induced lipid peroxidation as determined by the formation of thiobarbituric acid reactive substances in liver, kidneys and testes of rats. A 0.7% black tea extract was used which contained 2 mg of black tea extract solids per mL. Black tea was administered as drinking water for 3, 6, 9 and 12 months before and during carbon tetrachloride (CCl(4)) treatment in female and male rats. Rats were treated with a single oral dose of CCl(4) 1.0 mL/kg. All rats were killed 24 h after CCl(4) treatment. All animals were dosed with CCl(4) at the end of the 3, 6, 9, and 12 month of treatment. Black tea treatment for 75 days produced a decrease in CCl(4)-induced hepatic lipid peroxidation but significant decreases in thiobarbituric acid reactive substances occurred 3 months after treatment in both female and male rats. In liver and kidneys, black tea alone increased lipid peroxidation by 30%-50% in female and male rats. However, black tea decreased CCl(4)-induced lipid peroxidation in liver of female and male rats by approximately 49% and 37%, respectively. Black tea decreased CCl(4)-induced lipid peroxidation in testes by approximately 37% at a dose of 1.0 mL CCl(4)/kg. These results suggest that the protective effects of black tea against CCl(4)-induced lipid peroxidation in liver, kidneys and testes is due at least partly to its antioxidant properties, scavenging CCl(4)-associated free radicals.     

柴胡皂苷d抗肝纤维化大鼠脂质过氧化作用的研究

目的:探讨柴胡皂苷d(SSd)对肝纤维化过程中脂质过氧化的影响。方法:采用腹腔注射二甲基亚硝胺(DMN)10 mg.kg^-1诱导大鼠肝纤维化,以柴胡皂苷d(1.8 mg.kg^-1)同时预防给药4周,检测正常组、模型组和SSd组大鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、透明质酸(HA)、层粘连蛋白(LN)、IV型胶原(IV-C)及丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性及肝组织中MDA的含量和SOD的活性。结果:SSd能显著降低肝纤维化大鼠血清ALT,AST水平和HA,LN,IV-C的含量,并可提高肝组织中SOD的活性,降低血清和肝组织中的MDA的含量。结论:SSd具有很明显的保护肝细胞、抗肝纤维化的作用,其机制可能与抗脂质过氧化有关。     

丹酚酸B盐对大鼠纤维化肝组织脂质过氧化及其MMP-2活性的影响

目的:探讨丹酚酸B盐影响纤维化肝脏脂质过氧化与MMP-2活性的抗肝纤维化作用机制。方法:Wistar大鼠随机分为正常组、模型组、丹酚酸B盐组与培哚普利组。以二甲基亚硝胺腹腔注射复制肝纤维化模型,隔天1次,连续4周。丹酚酸B盐预防组与培哚普利对照组于造模开始即开始灌服,正常组与模型组大鼠给予等量生理盐水,连续4周。HE染色与胶原染色观察肝组织炎性坏死与胶原沉积;试剂盒检测血清肝功能(ALT,AST,Alb,T.Bil)与肝组织SOD活性、GSH含量与GST活性;盐酸水解法测定肝组织Hyp含量,Western blot检测I型胶原和α-SMA蛋白表达。明胶酶谱法检测肝组织MMP-2/9的活性。结果:模型大鼠肝脏有明显胶原沉积与肝纤维化,伴有明显肝细胞炎性损伤坏死;模型大鼠血清T.Bil含量、ALT与AST活性明显升高,血清Alb含量明显减少;肝组织Hyp含量、α-SMA与I型胶原蛋白、MMP-2活性明显增加,GSH含量、SOD与GST活性明显降低。丹酚酸B盐与培哚普利明显减轻肝纤维化模型大鼠的血清ALT水平与肝组织Hyp含量,抑制模型大鼠肝组织的α-SMA与I型胶原蛋白表达,以丹酚酸B盐作用明显,且均下调肝组织MMP-2活性,而增加SOD活性与GSH含量;丹酚酸B盐尚可降低模型大鼠血清T.Bil含量、提高肝组织GST活性。结论:改善纤维化肝脏的脂质过氧化损伤与降低肝组织MMP-2活性是丹酚酸B盐预防肝纤维化重要作用机制。     

雷公藤内酯醇对大鼠脑局灶性缺血再灌注脂质过氧化损伤影响的实验研究

 目的 观察雷公藤内酯醇(TL)对大鼠脑局灶性缺血再灌注脂质过氧化损伤影响。方法 预防性给予TL(0.2,0.4mg·kg^-1,腹腔注射)3 d,实验第4天制备大鼠局灶性脑缺血再灌注模型后仍同法腹腔注射TL。观察大鼠脑功能的变化及大脑中动脉闭塞侧脑皮质超微结构变化;检测大脑中动脉闭塞侧脑组织超氧化物歧化酶(SOD)、脂质过氧化物丙二醛(MDA)水平。结果 与损伤模型组比较,治疗组大鼠脑功能受损程度、大脑中动脉闭塞侧脑皮质电镜下神经细胞变性、坏死损伤程度明显改善;脑组织SOD水平显著升高、MDA水平显著下降。结论 TL对大鼠缺血再灌注脂质过氧化脑损伤有一定的保护作用。其作用机制可能与TL抗氧化作用有关。     

Effect of alcohol extract of Annona muricata on cold immobilization stress induced tissue lipid peroxidation

Administration of an ethanol extract of the stem bark of Annona muricata significantly inhibited cold immobilization stress-induced increase in lipid peroxidation in the liver and brain of albino rats. © 1997 John Wiley & Sons, Ltd.     

龙胆泻肝汤对氧自由基和由羟自由基诱导的脂质过氧化的影响

目的 探讨龙胆泻肝汤对氧自由基和由羟自由基诱导的批质过氧化的影响。方法 用邻苯三酚自氧化反应产生超氧阴离子自由基和Ｆｅｎｔｏｎ反应产生羟自由基,收羟自由基诱导大鼠虹膜睫状体组织匀浆的脂质过氧化反应。结果 龙胆泻肝汤对超氧阴离子自由基具有清除作用,并优于抗坏血酸;对羟自由基具有清除作用,对羟自由基诱导的批质过氧化具有抑制作用并强于甘露醇。结论 龙胆泻肝汤泻肝胆实火,清下焦湿热的机理可能与其清除氧自由     

Antiperoxidative effect of Livex,a herbal formulation against erythromycin estolate induced lipid peroxidation in rats

The present study was carried out to investigate the antiperoxidative effect of Livex, a compound herbal formulation, against erythromycin estolate induced lipid peroxidation. The oral administration of Livex to rats along with erythromycin estolate caused a significant reversal in lipid peroxidation, enzymatic leakage and produced enhancement of cellular antioxidant defence, revealing that the antioxidative action of Livex is responsible for its protective activity. These observations were supplemented by histopathological examination of liver and kidney sections. The results of this study revealed that Livex could afford significant protection against erythromycin estolate induced lipid peroxidation. Copyright © 1998 John Wiley & Sons, Ltd.     

盐酸千金藤碱对急性脂肪肝小鼠脂代谢及过氧化的影响

目的:探讨盐酸千金藤碱(CH)对小鼠急性脂肪肝的治疗作用及机制。方法:腹腔注射地塞米松(DXM)的同时灌服高脂饮食复制小鼠急性脂肪肝模型,应用不同剂量CH对其进行治疗,观察小鼠血脂及肝脂、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)等指标及肝脏病理学的影响。结果:与正常组相比,模型组小鼠血清甘油三酯(TG)、总胆固醇(TC)、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)活性和肝组织TG、TC、MDA含量显著升高(P<0.01),肝组织SOD和GSH-Px活性显著降低(P<0.01)。CH高剂量组小鼠血清TG、TC、ALT、AST及肝组织TG、TC、MDA显著低于模型组(P<0.01,P<0.05),肝组织SOD和GSH-Px活性显著高于模型组(P<0.01);不同剂量CH均能改善肝细胞脂肪变性情况。结论:CH对DXM所致小鼠急性脂肪肝具有良好的治疗作用,其机制可能与其能够提高抗氧化酶活性、抑制脂质过氧化反应等方面有关。     

A chemically characterized ethanolic extract of Thai Perilla frutescens (L.) Britton fruits (nutlets) reduces oxidative stress and lipid peroxidation in human hepatoma (HuH7) cells

Perilla frutescens is cultivated in East Asian countries including Thailand, and the nutlets (single‐seeded fruits) are used as traditional and medicinal food. Perilla nutlets extracted by ethyl acetate (EA), 80% ethanol (Eth), and hot water (HW) sequentially were chemically characterized using high‐resolution accurate liquid chromatography‐mass spectrometry with the main compounds detected assigned as rosmarinic acid and derivatives of the flavones apigenin and luteolin, with the more diverse chemical composition observed with the Eth extract. All extracts showed dose‐dependent free‐radical scavenging activity, with the Eth extract the most potent (IC₅₀ = 3.43 mg/ml for ABTS^? scavenging and 0.27 mg/ml for DPPH^? scavenging). The Eth extract also inhibited AAPH‐induced hemolysis (IC₅₀ = 0.07 mg/ml) more potently than did the HW (IC₅₀ = 0.38 mg/ml) and EA extracts (IC₅₀ = 1.63 mg/ml). An MTT test revealed all the extracts were noncytotoxic at concentrations up to 200 μg/ml. Only the Eth and EA extracts showed protective effects against the generation of reactive oxygen species and lipid peroxidation in FeCl₃‐induced HuH7 cells in a dose‐dependent manner. Our findings suggest the Eth extract of Thai perilla nutlets, containing rosmarinic acid and flavones and their derivatives, may have potential to provide protection against oxidative stress in hepatic disorders.     

温胆汤对代谢相关脂肪性肝病小鼠脂质代谢的影响

[目的] 探讨温胆汤对代谢相关脂肪性肝病（MAFLD）模型小鼠药物干预的作用及潜在的分子机制。[方法] 将44只C57BL/6J雄性无菌小鼠适应性饲养1周后随机分为6组,分别为空白组、模型组、温胆汤低剂量组（低剂量组）、温胆汤中剂量组（中剂量组）、温胆汤高剂量组（高剂量组）、吡咯列酮治疗组（吡咯列酮组）;实验小鼠给予高脂饲料进行MAFLD造模,每天分别灌胃给予低、中、高剂量组（1.3,2.6和5.2 g/kg）,吡格列酮组每天给予2.6 mg/kg。各干预治疗组小鼠均灌胃给药处理6周,每日1次。实验第14周末处死小鼠,比较6组小鼠肝指数、肝组织病理变化及脂肪含量,血清转氨酶、肝脏脂肪水平以及肝组织的氧化损伤指标丙二醛（MDA）,超氧化物歧化酶（SOD）水平和脂质代谢重要基因和蛋白,固醇调节元件结合蛋白-1c（SREBP-1c）、脂肪酸合成酶（FAS）、二酰基甘油酰基转移酶2（DGAT-2）、硬脂酰辅酶A去饱和酶1（SCD-1）、脂酰辅酶A氧化酶（ACO）的表达水平。[结果] 模型组与空白组比较,小鼠的整体状态差,肝脏组织大面积脂肪变性及脂质浸润,血清转氨酶、肝脏脂肪水平明显升高,证实了高脂饲料饮食喂养8周成功构建了小鼠MAFLD模型;各药物干预治疗组小鼠肝指数、肝脏病理变化和肝脏脂肪水平,血清转氨酶、脂质过氧化水平和脂质代谢重要基因和蛋白表达均较模型组显著降低,其中,高剂量组和吡咯列酮组下降最为明显,各组结果比较差异具有统计学意义（P<0.05）。[结论] 不同剂量温胆汤均能明显改善MAFLD小鼠肝脏脂质沉积、肝功能,降低肝指数,可能与调节脂质代谢,降低肝组织中脂质过氧化水平和脂质代谢重要基因的表达有关。