Effects of Beverages on Alcohol Metabolism: Potential Health Benefits and Harmful Impacts

Nonalcoholic beverages are usually consumed accompanying alcoholic drinks, and their effects on alcohol metabolism are unclear in vivo. In this study, the effects of 20 nonalcoholic beverages on alcohol metabolism and liver injury caused by alcohol were evaluated in mice. Kunming mice were orally fed with alcohol (52%, v/v) and beverages. The concentrations of ethanol and acetaldehyde in blood as well as the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in liver were assessed to indicate alcohol metabolism. The levels of aspartate aminotransferase (AST) and alanine transaminase (ALT) in serum as well as the levels of malonaldehyde (MDA) and superoxide dismutase (SOD) in liver were measured to reflect the alcohol-induced liver injury. The results showed that the treatment of soda water, green tea and honey chrysanthemum tea could accelerate ethanol metabolism and prevent liver injuries caused by alcohol when companied with excessive alcohol drinking. They might be potential dietary supplements for the alleviation of harmful effects from excessive alcohol consumption. On the contrary, some beverages such as fresh orange juice and red bull are not advised to drink when companied with alcohol consumption due to their adverse effects on ethanol induced liver injury.     

Hepatoprotective effect of Cassia obtusifolia seed extract and constituents against oxidative damage induced by tert‐butyl hydroperoxide in human hepatic HepG2 cells

The aim of the present study was to investigate the hepatoprotective effects of different soluble fractions of methanolic derived Cassia obtusifolia seeds extract (COE) and its active components in tert‐butyl hydroperoxide (t‐BHP)‐induced oxidative stress in HepG2 cells. Among the tested fractions, the ethyl acetate (EtOAc) fraction was the most active hepatoprotective fraction. From the active EtOAc fraction, six anthraquinones (alaternin, emodin, aloe emodin, 2‐hydroxyemodin 1‐methyl ether, chryso‐obtusin‐2‐O‐β‐d ‐glucoside, and questin) and one naphthopyrone glycoside (cassiaside) were isolated. The cytotoxic effect in 200 µM t‐BHP‐induced HepG2 cells was inhibited by COE and their bioactive compounds. The protective effect of COE in 200 µM t‐BHP‐induced HepG2 cells may be associated with positive regulation of glutathione (GSH) and decreased in reactive oxygen species (ROS) formation of their bioactive compounds. The increased ROS and decreased GSH levels observed in t‐BHP‐treated HepG2 cells were ameliorated by pretreatment with cassiaside, alaternin, and aloe emodin, indicating that the hepatoprotective effects of these major constituents are mediated by induction of cellular defense against oxidative stress. Overall, COE displayed a significant cytoprotective effect against oxidative stress, which may most likely be because of active compounds like cassiaside, alaternin, and aloe emodin in COE, which leads to maintenance of the normal redox status of cells.

Practical applications

The dried and roasted seeds of Cassia obtusifolia are commonly consumed as brew tea and medicinal foods in Korea. The seeds have multiple therapeutic actions related to the treatment of liver disease, dementia, diabetes, eye inflammation, photophobia and lacrimation, dysentery, headache, as well as dizziness. The present study demonstrates the hepatoprotective effect through prevention of oxidative stress, suggesting that C. obtusifolia and its constituents may have beneficial effects in preventing hepatic diseases.     

富硒玉米肽对四氯化碳致小鼠急性肝损伤的保护作用

研究富硒玉米肽对四氯化碳(Carbon tetrachloride,CCl4)诱导的小鼠肝损伤的保护作用。将健康的雄性昆明小鼠70只,随机分成7组:正常对照组、CCl4模型组、富硒玉米肽低、中、高剂量组(100、200、400mg/kg·bw)、普通玉米肽组(200 mg/kg·bw)、水飞蓟素阳性对照组(50 mg/kg·bw),每组10只。测定比较血清中谷丙转氨酶(ALT)活力、谷胱甘肽(GSH)、三酰甘油(TG)含量,同时测定肝组织中丙二醛(MDA)、谷胱甘肽(GSH)的含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力,肝脏指数,并观察肝组织病理学变化。结果显示富硒玉米肽低、中、高剂量组均能极显著抑制CCl4致肝损伤小鼠血清ALT活性和TG含量的升高、GSH含量的降低(P0.01);均能极显著提高肝组织中GSH含量和SOD、GSH-Px活力,并降低肝组织中MDA的含量(P0.01),极显著降低由于肝损伤引起的肝脏肿大(P0.01),改善肝组织损伤程度,并存在剂量效应关系。富硒玉米肽高剂量组的护肝效果与50 mg/kg·bw的水飞蓟素相当,相同剂量的富硒玉米肽的保肝作用极显著优于普通玉米肽(P0.01)。结果表明富硒玉米肽对CCl4所致小鼠急性肝损伤有显著的保护作用,且与普通玉米肽相比,富硒玉米肽的有效保肝剂量显著降低。     

紫草提取物对疲劳大鼠的肝组织保护作用

目的：通过观测耐力训练大鼠力竭和恢复24 h后肝组织及线粒体生化指标的变化,探讨紫草提取物在保肝护肝、提高运动能力、延缓运动疲劳、促进疲劳后恢复方面的生物学机理。方法：选取40 只Sprague-Dawley（SD）雄性大鼠,随机分为5 组,每组8只：训练对照组（A组）、运动力竭组（B组）、力竭恢复组（C组）、加药力竭组（D组）、加药恢复组（E组）。5 组大鼠按照训练模型进行为期6 周的跑台耐力训练,第6周的最后1 d,A组大鼠不进行训练,在安静状态下处死并进行样本处理和指标测定;B、C、D、E组大鼠进行一次性力竭运动后,处死B、D组大鼠并进行样本处理和指标测定;24 h后,处死C、E组大鼠并进行样本处理和指标测定。结果：大鼠在力竭运动后,肝组织抗氧化能力显著下降（P＜0.05）,一氧化氮合酶（nitric oxide synthase,NOS）活性和NO含量极显著降低（P＜0.01）,线粒体Na+/K+-ATPase、Ca2+/Mg2+-ATPase活性显著降低（P＜0.05）,24 h后,各指标恢复不明显。补充紫草提取物的大鼠在力竭运动后,与运动力竭组大鼠相比,肝组织抗氧化能力、NOS活性和NO含量、线粒体Na+/K+-ATPase、Ca2+/Mg2+-ATPase活性都显著升高（P＜0.05）;24 h后,各指标基本恢复到基础水平。结论：外源性补充紫草提取物可以有效调节NO的生成平衡,改善大鼠肝组织自由基清除和代谢水平,保护肝线粒体离子泵的活性和功能,能延缓运动疲劳的产生,促进运动后机体功能恢复。     

库拉索芦荟对黄曲霉毒素B1致大鼠急性肝损伤的保护作用

目的：研究库拉索芦荟在黄曲霉毒素B1（aflatoxin B1,AFB1）致大鼠急性肝损伤中的干预作用及机理。方法：采用单次灌胃2.0 mg/kg（以体质量计）AFB1建立大鼠急性AFB1肝损伤模型,通过体质量、肝功能指标、肝组织病理学变化评价库拉索芦荟的干预效果,并通过测定肝组织脂质过氧化产物、各抗氧化物水平,探讨库拉索芦荟拮抗急性AFB1肝毒性的作用机理。结果：库拉索芦荟具有显著降低急性AFB1肝毒性的功效,能有效抑制急性AFB1中毒大鼠体质量下降,降低血清谷丙转氨酶（glutamate pyruvate transaminase,GPT）、谷草转氨酶（glutamicoxalacetic transaminase,GOT）和碱性磷酸酶（alkaline phosphatase,ALP）活性以及总胆红素（total bilirubin,TBIL）含量;同时能显著改善肝脏组织病变情况,降低丙二醛（malondialdehyde,MDA）生成量,提高还原型谷胱甘肽（reduced glutathione,GSH）含量以及谷胱甘肽过氧化物酶（glutathione peroxidase,GSH-Px）、超氧化物歧化酶（superoxide dismutase,SOD）、谷胱甘肽-S-转移酶（glutathione-S-transferases,GST）活力,增强机体抗氧化及解毒能力。     

Modulation of Prostanoids Profile and Counter-Regulation of SDF-1α/CXCR4 and VIP/VPAC2 Expression by Sitagliptin in Non-Diabetic Rat Model of Hepatic Ischemia-Reperfusion Injury

Molecular mechanisms underlying the beneficial effect of sitagliptin repurposed for hepatic ischemia-reperfusion injury (IRI) are poorly understood. We aimed to evaluate the impact of IRI and sitagliptin on the hepatic profile of eicosanoids (LC-MS/MS) and expression/concentration (RTqPCR/ELISA) of GLP-1/GLP-1R, SDF-1α/CXCR4 and VIP/VPAC1, VPAC2, and PAC1 in 36 rats. Animals were divided into four groups and subjected to ischemia (60 min) and reperfusion (24 h) with or without pretreatment with sitagliptin (5 mg/kg) (IR and SIR) or sham-operated with or without sitagliptin pretreatment (controls and sitagliptin). PGI₂, PGE₂, and 13,14-dihydro-PGE₁ were significantly upregulated in IR but not SIR, while sitagliptin upregulated PGD₂ and 15-deoxy-12,14-PGJ₂. IR and sitagliptin non-significantly upregulated GLP-1 while Glp1r expression was borderline detectable. VIP concentration and Vpac2 expression were downregulated in IR but not SIR, while Vpac1 was significantly downregulated solely in SIR. IRI upregulated both CXCR4 expression and concentration, and sitagliptin pretreatment abrogated receptor overexpression and downregulated Sdf1. In conclusion, hepatic IRI is accompanied by an elevation in proinflammatory prostanoids and overexpression of CXCR4, combined with downregulation of VIP/VPAC2. Beneficial effects of sitagliptin during hepatic IRI might be mediated by drug-induced normalization of proinflammatory prostanoids and upregulation of PGD₂ and by concomitant downregulation of SDF-1α/CXCR4 and reinstating VIP/VCAP2 signaling.     

Antioxidant and Hepatoprotective Effects of Procyanidins from Wild Grape (Vitis amurensis) Seeds in Ethanol-Induced Cells and Rats

In the present study, we characterized the antioxidant and hepatoprotective mechanisms underlying of wild grape seed procyanidins (WGP) against oxidative stress damage in ethanol-treated HepG2 cell and Sprague-Dawley (SD)-rat models. In HepG2 cells, WGP not only diminished the ethanol (EtOH, 100 mM)-induced reactive oxygen species (ROS) formation and cytochrome P450 2E1 (CYP2E1) expression, but also renovated both the activity and expression of antioxidant enzymes including catalase, superoxide dismutase, and glutathione peroxidase. Additionally, to investigate the hepatoprotective effect of WGP, rats were orally administered 10 or 50 mg/kg WGP once daily for seven days prior to the single oral administration of EtOH (6 g/kg). The results show that WGP administration decreased the EtOH-induced augment of the levels of serum aspartate transaminase and alanine transaminase as well as serum alcohol and acetaldehyde. WGP treatment upregulated the activities and protein levels of hepatic alcohol dehydrogenase, aldehyde dehydrogenase, and antioxidant enzymes but downregulated the protein expression level of liver CYP2E1 in EtOH-treated rats. Moreover, the decreased phosphorylation levels of mitogen activated protein kinases (MAPKs) by ethanol were induced in both HepG2 cell and rat models. Overall, pretreatment of WGP displayed the protective activity against EtOH-mediated toxicity through the regulation of antioxidant enzymes and alcohol metabolism systems via MAPKs pathways.