Protective effects of saponins from the root of Platycodon grandiflorum against fatty liver in chronic ethanol feeding via the activation of AMP-dependent protein kinase

Fatty liver and steatosis induced by alcohol is the earliest and most common response of the liver to alcohol and may be a precursor of more severe forms of liver injury. However, the mechanism of liver injury and deposition of fatty liver due to alcohol is complex. The protective effects of saponins from the root of Platycodon grandiflorum (Changkil saponins: CKS) against ethanol-induced liver injury in an enteral alcohol feeding model was investigated. Male Sprague–Dawley rats were given control diets or ethanol-containing diets enterally for 4 weeks. Treatment with CKS for 2 weeks significantly prevented the alcohol-induced increase in serum alanine aminotransferase and aspartate aminotransferase activities or decrease in serum albumin levels. Alcohol elevated the hepatic triglyceride content and induced cytochrome P450 2E1 (CYP2E1) expression. CKS treatment reduced CYP2E1 expression and hepatic triglyceride accumulation and prevented alcoholic liver steatosis. Chronic alcohol feeding decreased AMP-activated protein kinase-alpha (AMPKα) phosphorylation, which was restored by CKS treatment. Recovery of AMPKα phosphorylation by CKS was also followed by an increase in acetyl-CoA carboxylase phosphorylation. Our study suggests that CKS is a promising agent for preventing or treating human alcoholic fatty liver disease.     

Platycodin D,a triterpenoid sapoinin from Platycodon grandiflorum, ameliorates cisplatin-induced nephrotoxicity in mice

Platycodin D (PD) is well known as a potent triterpenoid saponin having various pharmacological activities isolated from the root of Platycodon grandiflorum (Jacq.) A. DC. (Campanulaceae). We aimed to evaluate protective effect of PD on cisplatin (CDDP)-induced nephrotoxicity. Male ICR mice were allocated into five groups as follows: Negative control, CDDP alone and CDDP with PD (0.1, 1 and 5 mg/kg) treated group. PD was given for three consecutive days before CDDP injection. Increased blood urea nitrogen (BUN) and creatinine (CRE) levels in CDDP alone treated mice were decreased to normal range by pretreatment with PD. It also decreased nitric oxide (NO) and lipid peroxidation with increased antioxidant enzymes such as glutathione (GSH), glutathione peroxidase (GPx) and superoxide dismutase (SOD) in PD pretreated mice. In histopathological examination, pretreatment with PD showed ameliorated renal injury such as intraluminal cast formation and epithelial desquamation. Furthermore, over-expression of nuclear factor-kappa B p65 and apoptotic cells were suppressed by PD pretreatment. Taken together, PD pretreatment might be beneficial to CDDP-induced nephrotoxicity.     

Protective effect of saponins derived from the roots of Platycodon grandiflorum against carbon tetrachloride induced hepatotoxicity in mice

The purpose of this study was to investigate the protective effects of the saponins isolated from the root of Platycodi Radix (Changkil saponins: CKS) on carbon tetrachloride (CCl(4))-induced hepatotoxicities in mice. Pretreatment with CKS prior to the administration of CCl(4) significantly prevented the increase in serum alanine aminotransferase and aspartate aminotransferase activities and hepatic lipid peroxidation formation. In addition, CKS prevented CCl(4)-induced apoptosis and necrosis, as indicated by a liver histopathologic study and DNA laddering. To determine whether Fas/Fas ligand (FasL) pathway involved in CCl(4)-induced acute liver injury, Fas and FasL proteins and caspase-3, -8 activities were tested by western blotting and ELISA. CKS markedly decreased CCl(4)-induced Fas/FasL protein expression levels and in turn attenuated CCl(4)-induced caspase-3, -8 activities in mouse livers. Additionally, CKS protected the CCl(4)-induced depletion of hepatic glutathione levels. The effect of CKS on CYP2E1, the major isozyme involved in CCl(4) bioactivation, was investigated. Treatment with CKS resulted in a significant decrease in the CYP2E1-dependent hydroxylation of aniline. In addition, CKS exhibited antioxidant effects on FeCl(2)-ascorbate induced lipid peroxidation in liver homogenates, and on superoxide radical scavenging activity. These findings suggest that the protective effects of CKS against CCl(4)-induced acute liver injury possibly involve mechanisms related to its ability to block CYP2El-mediated CCl(4) bioactivation and its free radical scavenging effects, and that is also protects against Fas/FasL pathway mediated apoptosis.     

Inhibition of acrolein-stimulated MUC5AC expression by Platycodon grandiflorum root-derived saponin in A549 cells

Mucin overproduction is a hallmark of chronic airway diseases such as chronic obstructive pulmonary disease. In this study, we investigated the inhibition of acrolein-induced expression of mucin 5, subtypes A and C (MUC5AC) by Changkil saponin (CKS) in A549 cells. Acrolein, a known toxin in tobacco smoke and an endogenous mediator of oxidative stress, increases the expression of airway MUC5AC, a major component of airway mucus. CKS, a Platycodon grandiflorum root-derived saponin, inhibited acrolein-induced MUC5AC expression and activity, through the suppression of NF-κB activation. CKS also repressed acrolein-induced phosphorylation of ERK1/2, JNK1/2, and p38MAPK, which are upstream signaling molecules that control MUC5AC expression. In addition, the MAPK inhibitors PD98059 (ERK1/2), SP600125 (JNK1/2), and SB203580 (p38 MAPK), and a PKC delta inhibitor (rottlerin; PKCδ) inhibited acrolein-induced MUC5AC expression and activity. CKS repressed acrolein-induced phosphorylation of PKCδ. Moreover, a reactive oxygen species (ROS) inhibitor, N-acetylcysteine, inhibited acrolein-induced MUC5AC expression and activity through the suppression of PKCδ and MAPK activation, and CKS repressed acrolein-induced ROS production. These results suggest that CKS suppresses acrolein-induced MUC5AC expression by inhibiting the activation of NF-κB via ROS-PKCδ-MAPK signaling.     

Inhibitory mechanism of saponins derived from roots of Platycodon grandiflorum on anaphylactic reaction and IgE-mediated allergic response in mast cells

The purpose of this study was to investigate the protective effects of saponins isolated from the root of Platycodi Radix (Changkil saponins: CKS) anti-allergic effects in mice and mast cells. Oral administration of CKS inhibited the dinitrophenyl (DNP)–IgE antibody-induced systemic PCA reaction in mice. CKS reduced the β-hexosaminidase and histamine release from anti-DNP–IgE-sensitized RBL–2H3 cells. In addition, CKS inhibited the IgE antibody-induced increases in IL-4 and TNF-α production and expression in RBL-2H3 cells. In order to explore the inhibitory mechanism of CKS in PCA and mast cell degranulation, we examined the activation of intracellular signaling molecules. CKS suppressed DNP–IgE antibody-induced Syk phosphorylation. Further downstream, CKS also inhibited the phosphorylation of Akt and MAP kinases. Taken together, the in vivo/in vitro anti-allergic effects of CKS suggest possible therapeutic applications for this agent in allergic diseases through the inhibition of inflammatory cytokines and Syk-dependent signaling cascades.     

Protective effect of the Aralia continentalis root extract against carbon tetrachloride-induced hepatotoxicity in mice

The root of Aralia continentalis Kitagawa has been used in traditional Korean medicine to relieve pain and to treat inflammation. The purpose of this study was to investigate the protective effects of the extract of A. continentalis roots (AC) against hepatotoxicity induced by carbon tetrachloride (CCl₄) and the mechanism of its hepatoprotective effect. In mice, pretreatment with AC prior to the administration of CCl₄ significantly prevented the increased serum enzymatic activity of ALT and AST as well as the formation of hepatic malondialdehyde. Histopathological evaluation of the livers also revealed that AC reduced the incidence of liver lesions induced by CCl₄. In addition, pretreatment with AC significantly prevented both the depletion of reduced glutathione (GSH) content and the decrease in glutathione-S-transferase (GST) activity in the liver of CCl₄-intoxicated mice. Hepatic GSH levels and GST activity were increased by treatment with AC alone. Heme oxygenase-1 (HO-1) is known to be induced by oxidative stress and to confer protection against oxidative tissue injuries. Interestingly, AC markedly upregulated hepatic HO-1 expression in CCl₄-treated mice, which might provide anti-oxidative activity in the liver. These results indicate that AC plays a critical protective role in CCl₄-induced acute liver injury by promoting anti-oxidative protein expression.     

Deletion of circadian gene Per1 alleviates acute ethanol-induced hepatotoxicity in mice

The severity of ethanol-induced liver injury is associated with oxidative stress and lipid accumulation in the liver. Core circadian clock is known to mediate antioxidative enzyme activity and lipid metabolism. However, the link between circadian clock and ethanol-induced hepatotoxicity remains unclear. Here we showed that extents of acute ethanol-induced liver injury and steatosis in mice exhibit circadian variations consistent with hepatic expression of Period (Per) genes. Mice lacking clock gene Per1 displayed less susceptible to ethanol-induced liver injury, as evidenced by lower serum transaminase activity and less severe histopathological changes. Ethanol-induced lipid peroxidation was alleviated in Per1?/? mice. However, Per1 deletion had no effect on antioxidants depletion caused by ethanol administration. Ethanol-induced triglycerides (TG) accumulation in the serum and liver was significantly decreased in Per1?/? mice compared with that in wild-type (WT) mice. Analysis of gene expression in the liver revealed peroxisome proliferators activated receptor-gamma (PPARγ) and its target genes related to TG synthesis are remarkably down-regulated in Per1?/? mice. HepG2 cells were treated with ethanol at 150 mM for 3 days. Per1 overexpression augmented lipid accumulation after treatment with ethanol in HepG2 cells, but had no effect on ethanol-induced oxidative stress. Expression of genes related to lipogenesis, including PPARγ and its target genes, was up-regulated in cells overexpressing Per1. In conclusion, these results indicated that circadian rhythms of ethanol-induced hepatotoxicity are controlled by clock gene Per1, and deletion of Per1 protected mice from ethanol-induced liver injury by decreasing hepatic lipid accumulation.     

不同加工方法对桔梗根中多糖含量的影响

目的了解不同加工方法对桔梗多糖含量的影响。方法采用苯酚-硫酸法测定多糖的含量。结果不同干燥方法间桔梗多糖含量差异显著,依次为：切片干燥〉去皮干燥〉带皮干燥;桔梗鲜根收获后多糖含量随着放置时间的延长显著降低;鲜根放置去皮与否对多糖含量无显著影响。结论为保证桔梗根中多糖含量,桔梗鲜根收获后应及时切片烘干。     

Agrimonia eupatoria protects against chronic ethanol-induced liver injury in rats

This study examined the hepatoprotective effects of Agrimonia eupatoria water extract (AE) against chronic ethanol-induced liver injury. Rats were fed a Lieber–DeCarli liquid diet for 8 weeks. Animals were treated orally with AE at 10, 30, 100, and 300 mg/kg/day. After chronic consumption of ethanol, serum aminotransferase activities and pro-inflammatory cytokines markedly increased, and those increases were attenuated by AE. The cytochrome P450 2E1 activity and lipid peroxidation increased after chronic ethanol consumption, while reduced glutathione concentration decreased. Those changes were attenuated by AE. Chronic ethanol consumption increased the levels of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 protein expression, inducible nitric oxide synthase and cyclooxygenase-2 protein and mRNA expression, and nuclear translocation of nuclear factor-kappa B, which was attenuated by AE. Our results suggest that AE ameliorates chronic ethanol-induced liver injury, and that protection is likely due to the suppression of oxidative stress and TLR-mediated inflammatory signaling.     

桔梗总皂苷对左氧氟沙星在小鼠体内的药动学及组织分布的影响

目的 采用高效液相色谱（HPLC）法测定小鼠血浆及组织中左氧氟沙星含量,研究桔梗总皂苷对其药动学规律及组织分布的影响。方法 180只昆明小鼠随机分为两组,组Ⅰ为单独ig左氧氟沙星78 mg/kg,组Ⅱ为同时ig桔梗总皂苷65 mg/kg与左氧氟沙星78 mg/kg,采用HPLC法测定给药5、15、30、45 min及1、1.5、2、4、8 h后的血浆及肝、肺、肾组织样品中的左氧氟沙星浓度。结果 血浆中内源性物质对待测物无干扰;血浆及各组织在检测浓度范围内呈良好线性关系（r²>0.999）;方法日内和日间精密度、稳定性及提取回收率均符合生物样品检测标准;组ⅠAUC_0-t为（143.593±16.56）,组ⅡAUC_0-t为（120.339±15.542）,与组Ⅰ比较,组Ⅱ的AUC明显减小,T_1/2Z显著缩短,T_max明显延长,CLz/F显著增加,C_max及Vz/F无显著性差异;肝、肺、肾组织中左氧氟沙星浓度均迅速提高并快速消除,肺组织中消除速度最快,肺中AUC减少最为明显。结论 合用时,桔梗总皂苷使左氧氟沙星在小鼠体内消除速率明显加快,肺组织中尤为明显,故左氧氟沙星在联合含有桔梗成分的中药治疗肺部疾病时,建议分开服用。     

Influence of GSTs, CYP2E1 and mEH polymorphisms on 1, 3-butadiene-induced micronucleus frequency in Chinese workers

1,3-butadiene (BD) has been classified as a human carcinogen, however, the relationship between chromosomal damage and its metabolic polymorphisms is not clear. The present study used the CBMN assay to detect chromosomal damage in the peripheral lymphocytes of 166 exposed workers and 41 non-exposed healthy individuals. PCR and PCR-RFLP were applied to detect GSTT1, GSTM1, CYP2E1 c1c2 and mEH Tyr113His, His139Arg polymorphisms. The results demonstrated that the micronucleus (MN) frequency of the exposed workers was significantly higher than controls (P < 0.01). Among the exposed workers, the individuals with high BD exposures are more susceptible to chromosomal damage than those with low exposures (FR = 1.30, 95% CI 1.14-1.53; P < 0.05). Gender-difference was also found in our study: males got lower micronucleus frequency than females. Workers who carried the genotypes of GSTM1 (+), CYP2E1 (c1c2/c2c2) and mEH intermediate (I) group had significantly higher MN frequency than those carrying the genotypes of GSTM1 (−) (FR = 1.29, 95% CI 1.05-1.59; P < 0.05), CYP2E1 (c1c1) (FR = 1.55, 95% CI 1.24-1.93; P < 0.01) or mEH high (H) group (FR = 1.57, 95% CI 1.08-2.34; P < 0.05), respectively. Our data indicated that the current BD exposure level could cause significantly higher MN frequency in workers than controls. Polymorphisms of GSTM1, CYP2E1 and mEH are susceptible to altered chromosome damage.     

Preliminary characterization,antioxidant activity in vitro and hepatoprotective effect on acute alcohol-induced liver injury in mice of polysaccharides from the peduncles of Hovenia dulcis

The fresh fleshy peduncles of Hovenia dulcis have been used as a food supplement and traditional herbal medicine for the treatment of liver diseases and alcoholic poisoning for more than a millennium. The objectives of the present study, therefore, were to determine the antioxidant activity of polysaccharides from the peduncles of H. dulcis (HDPS) and to evaluate its hepatoprotective effect on acute alcohol-induced liver injury in mice. HDPS, prepared by hot water extraction, ethanol precipitation and treatment of macroporous resin, was found to be non-starch polysaccharide and mainly composed of galactose, arabinose, rhamnose and galacturonic acid. In in vitro antioxidant assay, HDPS exhibited high superoxide radical scavenging activity, strong inhibition effect on lipid peroxidation and a medium ferrous ion-chelating activity. For hepatoprotective activity in vivo, the administration of HDPS significantly decreased the serum levels of alanine aminotransferase and aspartate aminotransferase, significantly decreased the liver level of malondialdehyde and remarkably restored the liver activities of superoxide dismutase and glutathione peroxidase in alcohol-induced liver injury mice. The results suggested that HDPS had a significant protective effect against acute alcohol-induced liver injury possibly via its antioxidant activity to protect biological systems against the oxidative stress.     

Protective effects of Dunaliella salina – A carotenoids-rich alga,against carbon tetrachloride-induced hepatotoxicity in mice

The protective effects of Dunaliella salina (D. salina) on liver damage were evaluated by carbon tetrachloride (CCl₄)-induced hepatotoxicity in mice. Male ICR mice were orally treated with D. salina or silymairn daily with administration of CCl₄ twice a week for 8 weeks. CCl₄ induced liver damage and significantly (p < 0.05) increased the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in serum and decreased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), and GSH content in liver whereas increased hepatic malondialdehyde (MDA) content as compared with control group. Treatment with D. salina or silymarin could significantly (p < 0.05) decrease the ALT, AST, and ALP levels in serum and increase the activities of SOD, catalase, GSH-Px, glutathione reductase, and GSH content and decrease the MDA content in liver when compared with CCl₄-treated group. Liver histopathology also showed that D. salina reduced the incidence of liver lesions induced by CCl₄. The results suggest that D. salina exhibits potent hepatoprotective effects on CCl₄-induced liver damages in mice, and that the hepatoprotective effects of D. salina may be due to both the increase of antioxidant enzymes activities and inhibition of lipid peroxidation.     

Protective effect of Acacia confusa bark extract and its active compound gallic acid against carbon tetrachloride-induced chronic liver injury in rats

Acacia confusa Merr. (Leguminosae), a species native to Taiwan, is widely distributed on the hills and lowlands of Taiwan, and has been traditionally used as a medicine. The hepatoprotective effects of A. confusa bark extract (ACBE) and its active constituent gallic acid were evaluated against carbon tetrachloride (CCl₄)-induced hepatotoxicity in rats. CCl₄-induced hepatic pathological damage and significantly increased the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and malondialdehyde (MDA) in plasma, and cytochrome P4502E1 (CYP2E1) protein expression in hepatic samples, and decreased the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) in erythrocytes. Treatment with ACBE, gallic acid or silymarin could decrease significantly the AST, ALT, and MDA levels in plasma, and CYP2E1 expression in liver tissues, and increase the activities of SOD and GPX in erythrocyte when compared with CCl₄-treated group. Liver histopathology also showed that ACBE, gallic acid or silymarin could significantly reduce the incidence of liver lesions induced by CCl₄. These results suggested that the ACBE and gallic acid exhibit potent hepatoprotection against CCl₄-induced liver damages in rats, and the hepatoprotective effects of ACBE and gallic acid may be due to the modulation of antioxidant enzymes activities and inhibition of lipid peroxidation and CYP2E1 activation.     

Ability of Lactobacillus casei and Lactobacillus reuteri to protect against oxidative stress in rats fed aflatoxins-contaminated diet

Lactic acid bacteria (LAB) have been reported to remove mycotoxins from aqueous solutions through a binding process, which appears to be species and strain specific. The aim of the current study was to evaluate the protective role of Lactobacillus casei (L1) and Lactobacillus reuteri (L2) against aflatoxin (AFs)-induced oxidative stress in rats. Sixty female Sprague-Dawley rats were divided into 6 groups including the control group and the groups treated with L1 or L2 (1 × 10¹¹/ml) alone at a dose of 10 ml/kg b.w or plus AFs (3 mg/kg diet) for 4 weeks. At the end of the treatments, blood and tissue samples were collected for biochemical and histological studies. The results indicated that AFs alone induced a significant decrease in food intake and body weight and a significant increase in transaminase, alkaline phosphatase cholesterol, triglycerides, total lipids, creatinine, uric acid and nitric oxide in serum and lipid peroxidation in liver and kidney accompanied with a significant decrease in total antioxidant capacity. Treatments with L1 or L2 succeeded to induce a significant improvement in all the biochemical parameters and histological picture of the liver. Moreover, L2 was more effective than L1 and both can be used safely in functional foods.     

A novel TTX-producing Aeromonas isolated from the ovary of Takifugu obscurus

Puffer fish (Takifugu obscurus) from the Yangtze River of China were screened for tetrodotoxin-producing bacteria. An Aeromonas strain was isolated from the ovary of the puffer fish and was shown to produce tetrodotoxin; this strain was denoted Ne-1. The identity of tetrodotoxin produced by strain Ne-1 was confirmed by mouse bioassay, high performance liquid chromatography coupled with mass chromatography (LC-MS), and ELISA. Strain Ne-1 was characterized morphologically, biochemically, and by 16S rDNA phylogenetic analysis; these analyses suggested that strain Ne-1 is closely related to Aeromonas molluscorum. Given that strain Ne-1 was isolated from the ovary of T. obscurus, we propose that the TTX-producing Aeromonas sp. is a parasite or symbiotic bacterium rather than a sample contaminant. Collectively, our studies suggest that Aeromonas sp. strain Ne-1 produces tetrodotoxin in T. obscurus.     

Diphlorethohydroxycarmalol, isolated from the brown algae Ishige okamurae, protects against radiation-induced cell damage in mice

The aim of this study was to evaluate the radioprotective effects of diphlorethohydroxycarmalol (DPHC), isolated from the brown algae Ishige okamurae, in mice subjected to gamma irradiation.DPHC significantly decreased the level of radiation-induced intracellular reactive oxygen species in cultured Chinese hamster lung fibroblast (V79-4) cells (p < 0.05), enhanced cell viability that decreased after exposure to γ-rays, and reduced radiation-induced apoptosis in the V79-4 cells.Pretreatment with DPHC (100 mg/kg) in mice prior to irradiation significantly protected the intestinal crypt cells in the jejunum (p < 0.01) and maintained villi height (p < 0.01), compared with those of the vehicle-treated irradiated group. Mice pretreated with DPHC also exhibited dose-dependent increases in the bone marrow cell viability. The dose-reduction factor for gamma irradiation in the DPHC-pretreated mice was 2.05 at 3.5 days after irradiation.These results suggest that DHPC plays a role in protecting cells from irradiation-induced apoptosis, through the scavenging of reactive oxygen species in vitro, and that DPHC significantly protected intestinal progenitor cells and bone marrows cells that were decreased by gamma irradiation in vivo.     

Hepatoprotective effects of dieckol-rich phlorotannins from Ecklonia cava, a brown seaweed,against ethanol induced liver damage in BALB/c mice

Alcoholic liver disease, which is one of the most serious liver disorders, has been known to cause by ethanol intake. In the present study, in vivo hepatoprotective effects of dieckol-rich phlorotannins (DRP) from Ecklonia cava, a brown seaweed, on ethanol induced hepatic damage in BALB/c mice liver were investigated. After administration of 5 and 25 mg/kg mouse of DRP and 4 g/kg mice ethanol, the body weights and survival rates were increased as compared to the control, which is ethanol-treated group without DRP. The glutamic oxaloacetic transaminase and glutamic pyruvic transaminase levels in the serum were lower than those of the control. DRP exhibited a reduction of the total cholesterol. The lower levels of SOD enzyme and a reduction of the formation of malondialdehyde were occurred in mice fed with 5 and 25 mg/kg mouse of DRP. Finally the effect on improvement of fatty liver induced by ethanol was observed by taking out the liver immediately after dissecting the mouse. However, no significant difference was observed on hepatic histopathological changes. In conclusion, this study indicated that DRP could protect liver injury induced by ethanol in vivo. It suggested that DRP possesses the beneficial effect to human against ethanol-induced liver injury.     

Salvianolic acid B protects against acute ethanol-induced liver injury through SIRT1-mediated deacetylation of p53 in rats

Salvianolic acid B (SalB) is isolated from the traditional Chinese medical herb salvia miltiorrhiza. It has many biological and pharmaceutical activities. This study aimed to investigate the effect of SalB on acute ethanol-induced hepatic injury in rats and to explore the role of SIRT1 in this process. The results showed that pretreatment with SalB significantly reduced ethanol-induced elevation in aminotransferase activities, decreased hepatotoxic cytokine levels such as Interleukin-6 (IL-6), and increased the antioxidant enzyme activity. Moreover, SalB pretreatment reversed the increase in NF-κB, cleaved caspase-3 and decrease in B-cell lymphoma-extra large (Bcl-xL) caused by ethanol exposure. Importantly, SalB pretreatment significantly increased the expression of SIRT1, a NAD⁺-dependent deacetylase, whereas the increase in SIRT1 was accompanied by decreased acetyl-p53 expression. In HepG2 cells, SalB pretreatment increased SIRT1 expression in a time and dose-dependent manner and such an increase was abrogated by siRNA knockdown of SIRT1. Additionally, inhibition of SIRT1 significantly increased the acetylation of p53, and blocked SalB-induced acetylation of p53 down-regulation. Collectively, this study indicated that SalB can alleviate acute ethanol-induced hepatocyte apoptosis through SIRT1-mediated deacetylation of p53 pathway.