Beneficial effect of refined red palm oil on lipid peroxidation and monocyte tissue factor in HCV-related liver disease： a randomized controlled study

BACKGROUND： A large amount of endotoxin can be detected in the peripheral venous blood of patients with liver cirrhosis, contributing to the pathogenesis of hepatotoxicity because of its role in oxidative stress. The present study aimed to test the effect of the supplementation with red palm oil（RPO）, which is a natural oil obtained from oil palm fruit（Elaeis guineensis） rich in natural fat-soluble tocopherols, tocotrienols and carotenoids, on lipid peroxidation and endotoxemia with plasma endotoxin-inactivating capacity, proinflammatory cytokines profile, and monocyte tissue factor in patients with chronic liver disease. METHODS： The study group consisted of sixty patients（34 males and 26 females; mean age 62 years, range 54-75） with Child A/B, genotype 1 HCV-related cirrhosis without a history of ethanol consumption, randomly enrolled into an 8-week oral daily treatment with either vitamin E or RPO. All patients had undergone an upper gastrointestinal endoscopy 8 months before, and 13 out of them showed esophageal varices.RESULTS： Both treatments significantly decreased erythrocyte malondialdehyde and urinary isoprostane output, only RPO significantly affected macrophage-colony stimulating factor and monocyte tissue factor. Liver ultrasound imaging did not show any change. CONCLUSIONS： RPO beneficially modulates oxidative stress and, not least, downregulates macrophage/monocyte inflammatory parameters. RPO can be safely advised as a valuable nutritional implementation tool in the management of chronic liver diseases.

Heijiangdan Ointment(黑绛丹膏)Relieves Oxidative Stress from Radiation Dermatitis Induced by ^(60)Co γ-Ray in Mice

Objective：To investigate the effects of Heijiangdan Ointment（黑绛丹膏,HJD） on oxidative stress in （60）Co γ-ray radiation-induced dermatitis in mice.Methods：Female Wistar mice with grade 4 radiation dermatitis induced by ^（60）Co γ-rays were randomly divided into four groups（n=12 per group）;the HJD-treated,recombinant human epidermal growth factor（rhEGF）-treated,Trolox-treated,and untreated groups,along with a negative control group.On the 11 th and 21 st days after treatment,6 mice in each group were chosen for evaluation.The levels of superoxide dismutase（SOD）,malondialdehyde（MDA）,and lactate dehydrogenase（LDH） were detected using spectrophotometric methods.The fibroblast mitochondria were observed by transmission electron microscopy（TEM）.The expressions of fibroblast growth factor 2（FGF-2） and transforming growth factor β1（TGF-β1） were analyzed by western blot.Results：Compared with the untreated group,the levels of SOD,MDA and LDH,on the 11 th and 21 st days after treatment showed significant difference（P〈0.05）.TEM analysis indicated that fibroblast mitochondria in the untreated group exhibited swelling and the cristae appeared fractured,while in the HJD group,the swelling of mitochondria was limited and the rough endoplasmic reticulum appeared more relaxed.The expressions of FGF-2 and TGF-β1 increased in the untreated group compared with the negative control group（P〈0.05）.After treatment,the expression of FGF-2,rhEGF and Trolox in the HJD group were significantly increased compared with the untreated group（P〈0.05）,or compared with the negative control group（P〈0.05）.The expression of TGF-β1 showed significant difference between untreated and negative control groups（P〈0.05）.HJD and Trolox increased the level of TGF-β1 and the difference was marked as compared with the untreated and negative control groups（P〈0.05）.Conclusion：HJD relieves oxidative stress-induced injury,increases the antioxidant activity,mitigates the fibroblast mitochondrial damage,up-regulates the expression of growth factor,and promotes mitochondrial repair in mice.

Saeng-Kankunbi-Tang(生肝健脾汤) Protects Liver against Oxidative Damage through Activation of ERK/Nrf2 Pathway

Objective： To investigate the cytoprotective effects of Saeng-kankunbi-tang（生肝健脾汤, SKT）, a herbal prescription consisting of Artemisia capillaris and Alisma canaliculatum, and its underlying mechanism involved. Methods： In mice, blood biochemistry and histopathology were assessed in carbon tetrachloride（CCl4）-induced oxidative hepatic injury in vivo. The animal groups included vehicle-treated control, CCl4, SKT 500 mg/（kg·day） CCl4＋SKT 200 or 500 mg/（kg·day）. In Hep G2 cell, tert-butyl hydroperoxide（t BHP） induced severe oxidative stress and mitochondrial dysfunction in vitro. The cyto-protective effects of SKT were determined by 3-（4,5-dimethylthiazol）-2,5-diphenyltetrazolium bromide（MTT） assay, fluorescence activated cell sorting analysis and western blotting. Results： The administration of SKT prevented liver damage induced by CCl4 in mice, by inhibition of hepatocyte degeneration and inflammatory cell infiltration as well as plasma parameters such as alanine aminotransferase（P〈0.01）. Moreover, treatment with t BHP induced hepatocyte death and cellular reactive oxygen species production in hepatocyte cell line. However, SKT pretreatment（30–300 μg/m L） reduced this cell death and oxidative stress（P〈0.01）. More importantly, SKT inhibited the ability of t BHP to induce changes in mitochondrial membrane transition in cell stained with rhodamine 123（P〈0.01）. Furthermore, treatment with SKT induced extracellular signal-regulated kinases-mediated nuclear factor erythroid-2-related factor 2（Nrf2） activation as well as the expressions of heme oxygenase 1 and glutamate-cystein ligase catalytic, Nrf2 target genes. Conclusion： SKT has the ability to protect hepatocyte against oxidative stress and mitochondrial damage mediated by Nrf2 activation.