中药抗肝氧化应激的研究进展

回顾与总结近十年中药抗肝脏氧化应激的相关文献,为中药治疗肝氧化应激提供理论依据。以"肝(liver)""氧化应激(oxidative stress)""中药(Traditional Chinese Medicine)"为主题词,检索2002年以来的中文中国知网和英文PubMed数据库,综合文献并总结。中药对脂肪性肝病、病毒性肝炎、肝纤维化、肝癌及药物性肝病中的氧化应激均有作用。中药治疗肝氧化应激损伤具有一定的潜在应用价值,值得深入开发。

饮水氯化消毒副产物MX诱导人胚肝细胞氧化应激及其与DNA损伤的关系

目的研究饮水氯化消毒副产物3-氯-4-二氯甲基-5-羟基-2（5氢）-呋喃酮（MX）对体外培养的人胚胎肝细胞（L-02细胞）氧化应激的诱导。方法MX设10、30、100和300μmol／L4个暴露浓度，二甲基亚砜（DMSO，10ml／L）为溶剂对照，将L-02细胞染毒24小时后，检测L-02细胞内脂质过氧化产物丙二醛（MDA）、还原型谷胱甘肽（GSH）和8羟基脱氧鸟苷（8-OHdG）的含量。结果与溶剂对照相比，30、100和300μmol／L的MX能明显增加L02细胞MDA含量（P〈0．05，P〈0．001，P〈0．001），100、300μmol／L的MX使L02细胞GSH水平显著性降低（P〈0．001，P〈0．001）、8-OHdG含量显著性增加（P〈0．05，P〈0．01）。在MX0～300μmol／L浓度范围内，L-02细胞的MDA含量与8-OHdG含量呈正相关（r=0．767，P〈0．01）：GSH水平与8-OHdG含量呈负相关（r=0．761，P〈0．01）。结论MX可诱导L-02细胞氧化应激，使其脂质过氧化反应增强、抗氧化作用降低、DNA氧化损伤增加。MX引发的脂质过氧化反应和抗氧化力下降是DNA氧化损伤的影响因素之一。

黄芪提取物对铅中毒小鼠肝细胞氧化应激损伤的保护作用研究

目的:研究黄芪提取物对铅中毒小鼠肝细胞氧化应激损伤的保护作用。方法:将60只清洁级雄性昆明小鼠随机分为正常对照组(CG组)、模型组(MG组)、阳性药物组(PG组)、低剂量黄芪提取物组(LDG组)、中剂量黄芪提取物组(MDG组)和高剂量黄芪提取物组(HDG组)。向CG组小鼠的腹腔内注射生理盐水,向其余五组小鼠的腹腔内注射醋酸铅,20 d后对其进行灌胃建模。用纯化水为CG组小鼠与MG组小鼠灌胃,用DMSA为PG组小鼠灌胃,分别用低剂量、中剂量和高剂量的黄芪提取物为LDG组小鼠、MDG组小鼠和HDG组小鼠灌胃,然后比较六组小鼠的体重、肝脏系数、肝损伤的指标及其SOD、GSH-Px和MDA的水平。结果:CG组小鼠的体重高于其他五组小鼠,P <0.05。HDG组小鼠的体重高于LDG组小鼠和MDG组小鼠,P <0.05。MDG组小鼠的体重高于LDG组小鼠,P <0.05。CG组小鼠的肝脏系数低于其他五组小鼠,P <0.05。除CG组小鼠外其他五组小鼠的肝脏系数相比,P>0.05。HDG组小鼠的细胞膜损伤指数、细胞核移位指数和肝组织纤维化指数均低于LDG组小鼠与MDG组小鼠,P <0.05。MDG组小鼠的细胞膜损伤指数、细胞核移位指数和肝组织纤维化指数均低于LDG组小鼠,P <0.05。HDG组小鼠MDA的水平低于LDG组小鼠与MDG组小鼠,其SOD与GSH-Px的水平均高于LDG组小鼠与MDG组小鼠,P <0.05。MDG组小鼠MDA的水平低于LDG组小鼠,其SOD与GSH-Px的水平均高于LDG组小鼠,P <0.05。结论:黄芪提取物可减轻铅中毒小鼠肝细胞的氧化应激损伤,且浓度越高的黄芪提取物其作用效果越明显。

莱菔硫烷对汞致大鼠肝脏氧化应激的拮抗作用研究

目的探讨莱菔硫烷(sulforaphane,SFN)对汞所致肝脏氧化应激的拮抗作用。方法实验用Wistar大鼠60只,按体重随机分成6组:对照组,DMSO对照组,低、中、高剂量染汞组、SFN预处理组。对照组和染汞组皮下注射生理盐水,DMSO对照组皮下注射DMSO,SFN预处理组皮下注射2 mg/kg SFN;2 h后,对照组及DMSO对照组腹腔注射生理盐水,低、中、高剂量染汞组分别腹腔注射0.6、1.2、2.4 mg/kg Hg Cl2,SFN预处理组腹腔注射2.4 mg/kg Hg Cl2。注射容量为5 ml/kg。连续预处理与染毒3 d。于最后一次染汞24 h后,每组取6只大鼠,麻醉后处死,冰浴下切取肝组织,测定肝Hg含量、还原型谷胱甘肽(GSH)含量、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GPx)活力及丙二醛(MDA)含量。每组其余4只大鼠,制备肝脏单细胞悬液,测定肝细胞活性氧簇(ROS)及早期细胞凋亡率。结果与对照组比较,随染汞各组染Hg剂量的升高,肝组织Hg、GSH、MDA含量、肝细胞ROS水平及早期细胞凋亡率逐渐升高,SOD及GPx活力逐渐降低,呈现剂量-效应关系(P<0.01)。2.4 mg/kg Hg Cl2组肝组织Hg、GSH、MDA含量、肝细胞ROS水平及早期细胞凋亡率显著升高,SOD及GPx活力显著降低,差异有统计学意义(P<0.05或P<0.01)。SFN预处理组肝组织Hg含量与2.4 mg/kg Hg Cl2组相比未见明显差异(P>0.05),GSH、MDA含量、ROS水平及早期细胞凋亡率显著下降,SOD及GPx活力显著升高,差异有统计学意义(P<0.05或P<0.01)。结论 SFN对汞所致肝脏氧化应激具有一定程度的拮抗作用。

硫氧还蛋白与肝纤维化相关研究进展

肝纤维化是由各种原因引起慢性肝损伤的病理变化。它的特点是肝脏中细胞外基质(ECM)的过度积累,影响肝脏功能。肝纤维化的病因十分复杂,多种类型的慢性肝病均可以发展为肝纤维化。有关肝纤维化发病机制的研究主要集中在肝脏的炎症反应,氧化应激,肝细胞的生长和凋亡,以及肝星状细胞(HSC)的激活方面。

Pegylated interferon-alpha plus taurine in treatment of rat liver fibrosis

AIM: To investigate the antif ibrotic effects of peginterferon- alpha 2b and taurine on oxidative stress markers and hepatocellular apoptosis. METHODS: Sixty rats with CCl4-induced liver fibrosis were divided into 4 groups (n = 15). Group 1 was left for spontaneous recovery (SR). Groups 2-4 received peginterferon-alpha 2b, taurine, and their combination, respectively, for four weeks. Histological f ibrosis scores, histomorphometric analysis, tissue hydroxyproline, tissue MDA, GPx and SOD activities were determined. Activated stellate cells and hepatocellular apoptosis were also evaluated. RESULTS: The degree of f ibrosis decreased in all treatment groups compared to spontaneous recovery group. Taurine alone and in combination with peginterferon-alpha 2b reduced oxidative stress markers, but peginterferon-alpha 2b alone did not. Apoptotic hepatocytes and activated stellate cells were higher in groups 2-4 than in group 1. Combined taurine and peginterferon-alpha 2b further reduced fibrosis and increased activated stellate cell apoptosis, but could not improve oxidative stress more than taurine alone.CONCLUSION: Peginterferon-alpha 2b exerts anti- f ibrotic effects on rat liver fibrosis. It seems ineffective against oxidative stress in vivo. Peginterferon-alpha 2b in combination with taurine seems to be an antif ibrotic strategy.

Resveratrol attenuates oxidative stress and histological alterations induced by liver ischemia/reperfusion in rats

AIM： To investigate the effects of resveratrol on liver ischemia/reperfusion （I/R） injury in rats. METHODS： A total of 40 male Sprague-Dawley rats weighing 240-290 g were randomized into four groups of ten： （1） controls： data from unmanipulated animals; （2） sham group： rats subjected to the surgical procedure, except for liver I/R, and given saline; （3） I/R group： rats underwent liver ischemia for 45 rain followed by reperfusion for 45 rain; （4） I-R/Resveratrol group： rats pretreated with resveratrol （10 umol/L, iv）. Liver tissues were obtained to determine antioxidant enzyme levels and for biochemical and histological evaluation. RESULTS： Plasma aminotransferase activities were higher in the I/R group than in the I-R/Resveratrol group. Malondialdehyde levels and the hepatic injury score decreased, while superoxide dismutase, catalase, and glutathione peroxidase levels increased in group 4 compared to group 3. In group 4, histopathological changes were significantly attenuated in resveratroltreated livers. CONCLUSION： These results suggest that resveratrol has protective effects against hepatic I/R injury, and is a potential therapeutic drug for ischemia reperfusionrelated liver injury.

Relationship between oxidative stress and hepatic glutathione levels in ethanol-mediated apoptosis of polarized hepatic cells

AIM： To investigate the role of reactive oxygen species （ROS） in ethanol-mediated cell death of polarized hepatic （WlF-B） cells.METHODS： In this work, WIF-B cultures were treated with pyrazole （inducer of cytochrome P4502E1, CYP2E1） and/or L-buthionine sulfoximine （BSO）, a known inhibitor of hepatic glutathione （GSH）, followed by evaluation of ROS production, antioxidant levels, and measures of cell injury （apoptosis and necrosis）.RESULTS： The results revealed that ethanol treatment alone caused a significant two-fold increase in the activation of caspase-3 as well as a similar doubling in ROS. When the activity of the CYP2E1 was increased by pyrazole pretreatment, an additional two-fold elevation in ROS was detected. However, the CYP2EIrelated ROS elevation was not accompanied with a correlative increase in apoptotic cell injury, but rather was found to be associated with an increase in necrotic cell death. Interestingly, when the thiol status of the cells was manipulated using BSO, the ethanol-induced activation of caspase-3 was abrogated. Additionally, ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.CONCLUSION： Apoptotic cell death induced as a consequence of ethanol metabolism is not completely dependent upon ROS status but is dependent on sustained GSH levels,

Natural heme oxygenase-1 inducers in hepatobiliary function

Many physiological effects of natural antioxidants, their extracts or their major active components, have been reported in recent decades. Most of these compounds are characterized by a phenolic structure, similar to that of o-tocopherol, and present antioxidant properties that have been demonstrated both in vitro and in vivo. Polyphenors may increase the capacity of endogenous antioxidant defences and modulate the cellular redox state. Changes in the cellular redox state may have wide-ranging consequences for cellular growth and differentiation. The majority of in vitro and in vivo studies conducted so far have attributed the protective effect of bioactive polyphenols to their chemical reactivity toward free radicals and their capacity to prevent the oxidation of important intracellular components. However, in recent years a possible novel aspect inthe mode of action of these compounds has been suggested; that is, the ultimate stimulation of the heme oxygenase-1 （HO-1） pathway is likely to account for the established and powerful antioxidant/anti-inflammatory properties of these polyphenols. The products of the HO-catalyzed reaction, particularly carbon mon- oxide （CO） and biliverdin/bilirubin have been shown to exert protective effects in several organs against oxidative and other noxious stimuli. In this context, it is interesting to note that induction of HO-1 expression by means of natural compounds contributes to protection against liver damage in various experimental models. The focus of this review is on the significance of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against various stressors in several pathological conditions.

Bile acids:Chemistry,physiology,and pathophysiology

The family of bile acids includes a group of molecular species of acidic steroids with very peculiar physical-chemical and biological characteristics.They are synthesized by the liver from cholesterol through several complementary pathways that are controlled by mechanisms involving finetuning by the levels of certain bile acid species.Although their best-known role is their participation in the digestion and absorption of fat,they also play an important role in several other physiological processes.Thus,genetic abnormalities accounting for alterations in their synthesis,biotransformation and/or transport may result in severe alterations,even leading to lethal situations for which the sole therapeutic option may be liver transplantation.Moreover,the increased levels of bile acids reached during cholestatic liver diseases are known to induce oxidative stress and apoptosis,resulting in damage to the liver parenchyma and,eventually,extrahepatic tissues.When this occurs during pregnancy,the outcome of gestation may be challenged.In contrast,the physical-chemical and biological properties of these compounds have been used as the bases for the development of drugs and as pharmaceutical tools for the delivery of active agents.

Toxic Dinoflagellate Alexandrium tamarense Induces Oxidative Stress and Apoptosis in Hepatopancreas of Shrimp(Fenneropenaeus chinensis)

This study investigated the inductive effect ofAlexandrium tamarense, a toxic dinoflagellate producing paralytic shell- fish poison, on oxidative stress and apoptosis in hepatopancreas of Chinese shrimp, Fenneropenaeus chinensis. The individuals of E chinensis were exposed to 200 and 1000 cells mL-1 of A. tamarense with their superoxide dismutase （SOD）, glutathione S-transferase （GST） activities, malonyldialdehyde （MDA） concentration, and caspase gene （FcCasp） expression in hepatopancreas determined at 12, 24, 48, 72 and 96 h. In addition, apoptosis in hepatopancreas of E chinensis at 96 h after exposure was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） assay. The hepatopancreatic SOD and GST activities of F. chinensis exposed to 1000 cells mL-1 ofA. tamarense showed a bell-shaped response to exposure time. The hepatopancreatic MDA concentration ofF. chinensis exposed to 1000 cellsmL-1 ofA. tamarense increased gradually from 48 to 96h, and such a trend corresponded to the decrease of GST activity. The hepatopancreatic FcCasp transcript abundance of F. chinensis exposed to 1000 cells mL-1 ofA. tamarense was positively and linearly correlated to MDA concentration. Results of TUNEL assay showed that exposure to 1000 cells mL-1 of A. tamarense induced apoptosis in the hepatopancreas of E chinensis. Our study revealed that A. tamarense exposure influenced the antioxidative status ofF. chinensis and caused lipid peroxidation and apoptosis in the hepatopancreas of shrimp.

Liver Damage by the Interaction of Malathion with Cimetidine in Rat

In this study the authors aimed to evaluate the oxidative stress enzymes indicative of liver damage in rats exposed to malathion （M）, subchronic form using cimetidine （C） and cimetidine plus malathion （M ＋ C）. Malathion, widely used organophosphorus insecticide worldwide, induces oxidative liver damage type; cimetidine is an antagonist of histamine H2-receptor, it has been shown to be an inhibitor of various CYP45o isoforms. Male Wistar rats weighing 200-250 g were studied, exposed to malathion orally for 3 weeks （0.15 mg/kg/day, 2 mg/kg/day, 15 mg/kg/day） and cimetidine 10 mg/kg/day. Malathion plus cimetidine affect susceptibility to oxidative stress and possibly modifies the antioxidant defense capacity directly or indirectly.

染料木素及大豆苷元调控线粒体介导的细胞凋亡减轻京尼平诱导的肝细胞损伤

目的:通过探究淡豆豉主要药效成分染料木素、大豆苷元对栀子致毒成分京尼平所致HepG2细胞损伤的保护作用,进一步揭示栀子与淡豆豉配伍减毒的机制。方法:采用250μmol/L京尼平建立HepG2细胞损伤模型,将不同浓度染料木素、大豆苷元(0.5~10)μmol/L与京尼平共孵育于HepG2细胞,测定细胞存活率及氧化应激水平(胞内锰-超氧化物歧化酶Mn-SOD、过氧化氢酶CAT活力,谷胱甘肽GSH含量及活性氧ROS水平);高内涵技术(high content screening,HCS)检测线粒体功能(线粒体膜电位mitochondrial membrane potential,MMP和细胞色素C水平)及细胞凋亡情况;Western Blot法检测线粒体凋亡通路蛋白Bcl-2、Bax、Bcl-xL、Bik、Caspase-3表达水平。结果:与正常对照组比较,模型对照组细胞存活率显著下降(P<0.01);Mn-SOD、CAT活力及GSH水平显著降低(P<0.01);ROS释放量显著增加(P<0.01);细胞色素C水平及细胞膜通透性显著增加、MMP显著降低、细胞核固缩、浓染及细胞数量显著下降(P<0.01);Bax、Bik、Caspase 3蛋白表达水平显著上调,Bcl-2、Bcl-xL蛋白表达显著下调(P<0.01)。与模型对照组相比,1、2.5、5、10μmol/L染料木素、大豆苷元可明显升高细胞存活率(P<0.05或P<0.01);2.5、5、10μmol/L染料木素、大豆苷元可明显升高细胞Mn-SOD活力及GSH含量,2.5、5、10μmol/L染料木素及5、10μmol/L大豆苷元可显著升高细胞CAT活力(P<0.05或P<0.01)。5μmol/L染料木素、5μmol/L大豆苷元、2.5μmol/L染料木素+2.5μmol/L大豆苷元可使ROS释放量显著减少,细胞色素C含量和细胞膜通透性下降,MMP上升,显著改善核固缩及核内染色质凝集等凋亡情况(P<0.05或P<0.01);且Bcl-2、Bcl-xL蛋白表达显著上调,Bax、Bik、Caspase-3蛋白表达显著下调(P<0.01)。结论:染料木素和大豆苷元可通过保护线粒体,减少线粒体介导的细胞凋亡显著改善京尼平诱发的肝细胞损伤,栀子与淡豆豉配伍减毒的机制与此相关。

Anti-Acute Fatigue Effects of Ethanol Extract of Bidens pilosa L.and the Profiling of Antioxidant Index in ICR Mice

The effects of ethanol extract of Bidens pilosa L.(EEB)on acute exercise fatigue and its underlying biochemical mechanism were investigated in this study.Sixty adult male ICR mice were divided into control,model,vitamin C(VC)100,EEB40,EEB80,and EEB160 groups,receiving VC(100 mg/kg)or EEB(40,80,160 mg/kg)for 28 days(intragastrically,I.G.).The mice underwent tailsuspension,elevated plus maze(EPM),rotarod,and loaded swimming tasks and biochemical indices were measured.There were no significant differences in body weight,tail suspension time,EPM open arm time/entries and serum cortisone levels among the groups.Compared with the model group,there was an increase in rotarod latency in the VC100/EEB80 groups and an increase in loaded swimming time in the EEB80/EEB160 groups.Furthermore,the haptic and muscle glycogen levels decreased in the model group,while the haptic glycogen levels increased in the all VC/EEB groups.Similarly,the serum lactate and creatinine levels increased in the model group,but decreased in lactate(except for EEB160),creatinine(except for EEB40)and lactate dehydrogenase in the EEB80 group.In the liver,malonaldehyde(MDA)and oxidized glutathione(GSSG)levels increased in the model group;however,glutathione reductase(GR)(except for EEB40),glutathione(GSH)and GSH/GSSG ratios increased,with GSSG levels decreasing in all VC/EEB groups.In the quadriceps,the GR levels increased in the model,whereas it decreased in the VC100,EEB40 and EEB80 groups.These results suggest that EEB has anti-acute fatigue effect,potentially attributed to mitigate metabolite accumulation,enhancing glycogen reserves,and fortifying the antioxidant mechanism.

Protective effects of Polygonatum sibiricum against CCl_(4)-induced acute liver injury in rats through oxidative stress and mitochondrial apoptotic pathways

In the present study,we aimed to investigate the hepatoprotective effect of Chinese herbal medicine Polygonatum sibiricum(PS).In this study,a rat acute liver injury(ALI)model was established by a single intraperitoneal injection of 50%CCl_(4) oil solution,and the rats were treated intragastrically with Polygonatum sibiricum aqueous extract(PSAE).The results showed that PSAE significantly decreased the serum levels of ALT,AST and ALP,increased the activities of glutathione(GSH)and superoxide dismutase(SOD),decreased malondialdehyde(MDA)activity in hepatic tissue,and decreased the reactive oxygen species(ROS)level in hepatocytes.The expressions of Nrf2,NQO-1,HO-1,Bcl-2,Bcl-x L mRNA,and HO-1 proteins were elevated,and the expression of p53 mRNA was decreased.In conclusion,PSAE exerted a powerful protective action against CCl_(4)-induced ALI in rats via effectively regulating the expressions of Nrf2-Keap1-ARE related genes and proteins,and inhibiting hepatocyte apoptosis.These outcomes provided evidence that PS had apparent hepatoprotective effect.

The alleviating effect of quercetin on carbon tetrachloride-induced liver fibrosis in rats and its underlying mechanism

Quercetin, a phenolic phytochemical widely present in vegetables and fruits, has antioxidant, anti-inflammatory, antiviral, and immunomodulatory activities, and it has been successfully used in the treatment of acute and chronic diseases. In the present study, we aimed to investigate the alleviation effect of quercetin on rat liver fibrosis and explore its mechanism of action. Healthy male SD rats were randomly divided into the normal group, model group, and quercetin group, with six rats in each group. Liver fibrosis was induced by intraperitoneal injection of 1 m L/kg carbon tetrachloride(50% v/v in olive oil) twice a week for 6 weeks, and quercetin(100 mg/kg/d) was administered orally in the 7th week until the end of the 12th week. Blood and liver samples were collected at 1 h after the last administration. Serum liver function parameters(AST, ALT, ALP, GGT, and TBA) were detected by an automatic biochemical analyzer. H&E, Masson, and Sirius red staining were used to observe the pathological morphology of liver tissue. Western blotting analysis was used to evaluate the expressions of liver fibrotic factors(TGF-β1, α-SMA, MMP2, and MMP9) and bile acid-related regulatory proteins(FXR, CYP7A1, CYP8B1, and CYP27A1). The oxidative stress markers(GSH, GSH-Px, GR, SOD, and MDA) in the liver tissue were detected using corresponding kits. The contents of bile acids in the liver tissue were determined by LC-MS/MS. The results showed that compared with the model group, quercetin treatment could significantly reduce serum AST, ALT, and TBA levels(P < 0.05). The fibrotic liver injury was significantly improved, and the expressions of fibrotic factors TGF-β1, α-SMA, MMP2, and MMP9 were significantly decreased(P < 0.05). Liver GSH, GSH-Px, GR, and SOD levels were significantly increased(P < 0.05), and the MDA level was significantly decreased(P < 0.05). The contents of hepatic bile acids were significantly decreased(P < 0.05), the expression of FXR was significantly increased(P < 0.05), and the expressions of CYP7A1 and CYP8B1 were significantly decreased(P < 0.05). This study suggested that quercetin could effectively alleviate carbon tetrachloride-induced liver fibrosis injury, and its mechanism of action was related to improving the liver’s ability to resist oxidative stress and reducing the expressions of fibrotic factors and bile acid synthesis.

Dihydromyricetin improves liver fat deposition in high-fat diet-induced obese mice

It has been reported that the histone/protein deacetylase SIRT1-AMP-activated protein kinase(SIRT1-AMPK)signaling pathway may play a role in the effects of dihydromyricetin(DHM)on improving triglyceride(TG)accumulation and insulin resistance in liver cells.Therefore,we aimed to further observe the effect of DHM on liver fat deposition in high-fat diet(HFD)-induced obese mice and explore its possible mechanism.C57BL/6J mice were fed with a normal diet(ND)and HFD and were treated with or without low-dose(125 mg/kg)or high-dose(250 mg/kg)DHM for 16 weeks,respectively.During the experiment,body weight was checked every 2 weeks.After 16 weeks,the orbital vein was bled,the animals were sacrificed,and the subscapular,epididymal,and inguinal fat were collected and weighed with an electronic scale.An automatic biochemical analyzer was used to determine the levels of serum triglyceride(TG),serum total cholesterol(TC),serum high-density lipoprotein(HDL),and serum low-density lipoprotein(LDL).The livers were stained with hematoxylin-eosin staining(H&E)and Oil Red O to detect liver fat deposition.A colorimetric method was used to detect liver MDA and SOD contents.Quantitative real-time PCR(q RT-PCR)was used to detect the gene expressions of related indicators,such as interleukin-6(IL-6),interleukin-8(IL-8),tumor necrosis factor-α(TNF-α),acetyl-Co A carboxyl acetyl-Co A carboxylase(ACC),sterol regulatory element-binding protein-1c(SREBP-1),fatty acid synthetase(FAS),peroxisome proliferator activation receptor alpha(peroxisome proliferator-activated receptor-alpha,PPARα),palmitoyltransferase 1(carnitine palmitoyltransferase 1,CPT1),SIRT1,and AMPK.Western blotting analysis was used to detect the protein expression levels of SIRT1,AMPK,SIRT1-AMPK,ACC,SREBP-1,FAS,PPARα,and CPT1.Results showed that compared with the ND group,the weight and body fat of the mice in the HFD group were increased significantly.The levels of TG,TC,and LDL were increased,the level of HDL was decreased,the volume of hepatocytes was increased,the number of lipid droplets,fat deposition,MDA,IL-6,IL-8,TNF-α,SREBP-1c,FAS,ACC1,SIRT1,and AMPK protein levels were significantly increased,and the SOD activity,PPARα,CPT1,SIRT1 m RNA,AMPK m RNA,PPARα,CPT1 levels were significantly decreased.DHM could significantly reverse the changes of the above indexes in HFD mice,while DHM had no significant effect on the above indexes in ND mice.Collectively,our findings revealed that DHM improved liver fat deposition in HFD-induced obese mice,and the mechanism might be related to inhibition of oxidative stress,inflammation,lipid synthesis,and promotion of lipid decomposition.