Hepatoprotective Effects of Berberis vulgaris L. Extract/β Cyclodextrin on Carbon Tetrachloride-Induced Acute Toxicity in Mice

The present study investigated the capacity of formulated Berberis vulgaris extract/β-cyclodextrin to protect liver against CCl(4)-induced hepatotoxicity in mice. Formulated and non-formulated extracts were given orally (50 mg/kg/day) to mice for 7 days and were then intra-peritoneally injected with 1.0 mL/kg CCl(4) on the 8th day. After 24 h of CCl(4) administration, an increase in the levels of apartate-amino-transferase (AST), alanine-amino-transferase (ALT) and malondialdehyde (MDA) was found and a significant decrease in superoxide-dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione-peroxidase (GPx) levels could be detected. This was accompanied by extended centrilobular necrosis, steatosis, fibrosis and an altered ultrastructure of hepatocytes. Pre-treatment with formulated or non-formulated extract suppressed the increase in ALT, AST and MDA levels and restored the level of antioxidant enzymes at normal values. Histopathological and electron-microscopic examination showed milder liver damage in both pre-treated groups and the protective effect was more pronounced after the formulated extract was administered. Internucleosomal DNA fragmentation induced by CCl(4) was reduced in the group which received non-formulated extract and absent in the group which received formulated extract. Taken together, our results suggest that Berberis vulgaris/β-cyclodextrin treatment prevents hepatic injury induced by CCl(4) and can be considered for further nutraceutical studies.     

Ameliorative Effects of 5-Hydroxymethyl-2-furfural (5-HMF) from Schisandra chinensis on Alcoholic Liver Oxidative Injury in Mice

The aim of this paper is to evaluate the protective effect of 5-hydroxymethyl-2-furfural (5-HMF) on acute alcohol-induced liver oxidative injury in mice. 5-HMF, a maillard reaction product, was isolated from the fruits of Schisandra chinensis for animal experiments. Experimental ICR mice were pretreated with different doses of 5-HMF (7.5, 15, and 30 mg/kg) for seven days by gavage feeding. Biochemical markers and enzymatic antioxidants from serum and liver tissue were examined. Our results showed that the activities of ALT (alanine aminotransferase), AST (aspartate transaminase), TC (total cholesterol), TG (triglyceride), L-DLC (low density lipoprotein) in serum and the levels of MDA (malondialdehyde) in liver tissue, decreased significantly (p < 0.05) in the 5-HMF-treated group compared with the alcohol group. On the contrary, enzymatic antioxidants CAT (catalase), GSH-Px (glutathione peroxidase), and GSH SOD (superoxide dismutase) were markedly elevated in liver tissue treated with 5-HMF (p < 0.05). Furthermore, the hepatic levels of pro-inflammatory response marker tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) were significantly suppressed (p < 0.05). Histopathological examination revealed that 5-HMF (30 mg/kg) pretreatment noticeably prevented alcohol-induced hepatocyte apoptosis and fatty degeneration. It is suggested that the hepatoprotective effects exhibited by 5-HMF on alcohol-induced liver oxidative injury may be due to its potent antioxidant properties.     

治疗用卡介苗抗肿瘤动物实验方法的建立

目的 建立治疗用卡介苗在小鼠体内抗肿瘤的药效学实验方法。方法 观察治疗用卡介苗(BCG)对小鼠实体瘤S180和腹水瘤(EC)的抑瘤作用。结果BCG可明显减轻S180荷瘤鼠的瘤重,其瘤重抑制率>30％;可明显延长EC腹水瘤小鼠的生存时间,其生命延长率>75％。其中以12.5％和6.25mg/kg两剂量组的效果较佳。结论 该方法可用于卡介苗抗肿瘤动物药学实验。     

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.     

Effect of Dietary Protein Level and Origin on the Redox Status in the Digestive Tract of Mice

The present study was undertaken to evaluate the effects of high protein (soybean protein or casein) on the balance between production of free radicals and antioxidant level in digestive organs of mice. For this purpose, male (C57BL/6J) mice were adapted to experimental diets containing soybean protein or casein with 20% (normal protein diets, NPDs) or 60% (high protein diets, HPDs), and HPDs supplemented with 0.06g/kg cysteamine. After two weeks of feeding, oxidative and antioxidative parameters in duodenum, liver and pancreas were measured. The results show that ingestion of high protein markedly increased contents of superoxide anion and malondialdehyde (MDA), decreased activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and Na⁺ K⁺-ATPase, and content of reduced glutathione (GSH) in digestive organs of mice (P<0.05). Levels of oxidative parameters were lower and antioxidant capacity of both enzyme and non-enzyme was higher in mice fed with soybean protein than those fed with casein. In groups fed HPDs supplemented with cysteamine, oxidative stress was mitigated. However, oxidative parameter levels were still higher than those of NPD-fed groups. The present study indicates that ingestion of high protein diets could result in an imbalance between oxidant and antioxidant, and thus induce oxidative stress in digestive organs of mice. The oxidative damage was smaller in mice fed with high level of soy protein in comparison with casein.     

Antioxidant activity of tea extracts in lipids and correlation with polyphenol content

The present study examined the antioxidative activity of water and ethanol extracts of green and black tea leaves against the oxidation of heated sunflower oil and lard. Oxidation was conducted at 110 °C in the Rancimat test. Total polyphenols and catechin contents in tea extracts were measured. The research showed that the total polyphenol content in green and black tea leaves was 205.2 and 148.7 mg/g, respectively. In tea leaves extracts, it ranged between 245.9 mg/g and 837.7 mg/g and depended on the extraction solvent and the kind of tea used (p <0.001). The highest polyphenol content was observed in samples extracted with 95% ethanol, lower contents were found with the use of water. Results showed that the highest antioxidant activity, measured as an induction period, with 1000 ppm green tea ethanol extract, was comparable to á‐tocopherol activity in sunflower oil. In lard, the longest induction period was measured with 500 and 1000 ppm of green tea ethanol extract. Other tea extract concentrations were significantly less active. Statistical analysis of the tea extract antioxidant activity in lipids in the Rancimat test showed an essential influence of the catechin contents. Further statistical analysis also showed an influence of (?)‐epicatechin gallate (ECG), (?)‐epicatechin (EC), and (+)‐catechin (C) contents in the tea extracts on the antioxidant activity in lipids. It was stated that the antioxidant activity was higher in tea extracts containing high levels of ECG, EC, and C.     

Oxidative Stress and DNA Damage in Human Gastric Carcinoma: 8-Oxo-7′8-dihydro-2′-deoxyguanosine (8-oxo-dG) as a Possible Tumor Marker

We characterized the oxidative stress (OS) status by the levels of reduced/oxidized glutathione (GSH/GSSG), malondialdehyde (MDA) and the mutagenic base 8-oxo-7′8-dihydro-2′-deoxyguanosine (8-oxo-dG) in human gastric carcinoma (HGC) samples and compared the results with normal tissue from the same patients. We also analyzed 8-oxo-dG in peripheral mononuclear cells (PMNC) and urine from healthy control subjects and in affected patients in the basal state and one, three, six, nine and twelve months after tumor resection. The levels of DNA repair enzyme mRNA expression (hOGG1, RAD51, MUYTH and MTH1) were determined in tumor specimens and compared with normal mucosa. Tumor specimens exhibited increased levels of MDA and 8-oxo-dG compared with normal gastric tissue. GSH levels were also increased, while GSSG levels remained stable. DNA repair enzyme mRNA expression was induced in the tumor tissues. Levels of 8-oxo-dG were significantly elevated in both urine and PMNC of gastric cancer patients compared with healthy controls. After gastrectomy, the levels of the damaged base in urine and PMNC decreased progressively to values close to those found in the healthy population. The high levels of 8-oxo-dG in urine may be related to the increased induction of DNA repair activity in tumor tissue, and the changes observed after tumor resection support its potential use as a tumor marker.     

Comparative effects of palm vitamin E and α-tocopherol on healing and wound tissue antioxidant enzyme levels in diabetic rats

The effect of supplementing 200 mg/kg body weight palm vitamin E (PVE) and 200 mg/kg body weight α-tocopherol (α-loc) on the healing of wounds in streptozotocin-induced diabetic rats was evaluated. The antioxidant potencies of these two preparations of vitamin E were also evaluated by determining the antioxidant enzyme activities, namely, glutathione peroxidase (GPx) and superoxide dismutase (SOD), and malondialdehyde (MDA) levels in the healing of dermal wounds. Healing was evaluated by measuring wound contractions and protein contents in the healing wounds. Cellular redistribution and collagen deposition were assessed morphologically using cross-sections of paraffin-embedded day-10 wounds stained according to the Van Gieson method. GPx and SOD activities as well as MDA levels were determined in homogenates of day-10 dermal wounds. Results showed that PVE had a greater potency to enhance wound repair and induce the increase in free radical-scavenging enzyme activities than α-Toc. Both PVE and α-Toc, however, were potent antioxidants and significantly reduced the lipid peroxidation levels in the wounds as measured by the reduction in MDA levels.     

DADS Suppresses Human Esophageal Xenograft Tumors through RAF/MEK/ERK and Mitochondria-Dependent Pathways

Diallyl disulfide (DADS) is a natural organosulfur compound isolated from garlic. DADS has various biological properties, including anticancer, antiangiogenic, and antioxidant effects. However, the anticancer mechanisms of DADS in human esophageal carcinoma have not been elucidated, especially in vivo. In this study, MTT assay showed that DADS significantly reduced cell viability in human esophageal carcinoma ECA109 cells, but was relatively less toxic in normal liver cells. The pro–apoptotic effect of DADS on ECA109 cells was detected by Annexin V-FITC/propidium iodide (PI) staining. Flow cytometry analysis showed that DADS promoted apoptosis in a dose-dependent manner and the apoptosis rate could be decreased by caspase-3 inhibitor Ac-DEVD-CHO. Xenograft study in nude mice showed that DADS treatment inhibited the growth of ECA109 tumor in both 20 and 40 mg/kg DADS groups without obvious side effects. DADS inhibited ECA109 tumor proliferation by down-regulating proliferation cell nuclear antigen (PCNA). DADS induced apoptosis by activating a mitochondria-dependent pathway with the executor of caspase-3, increasing p53 level and Bax/Bcl-2 ratio, and downregulating the RAF/MEK/ERK pathway in ECA109 xenograft tumosr. Based on studies in cell culture and animal models, the findings here indicate that DADS is an effective and safe anti-cancer agent for esophageal carcinoma.     

The Role of Receptor for Advanced Glycation End Products (RAGE) in the Proliferation of Hepatocellular Carcinoma

The receptor for advanced glycation end products (RAGE) is oncogenic and overexpressed in human cancers, but its role in hepatocellular carcinoma remains unclear. Here we demonstrated that RAGE is overexpressed in primary hepatocellular carcinoma (PHC) compared to adjacent para-neoplastic liver samples. Serum endogenous secretory RAGE levels were also increased in PHC patients (p < 0.01). Moreover, we demonstrated that RAGE regulates cellular proliferation in Hepatocellular carcinoma (HCC). Knockdown of RAGE by specific siRNA inhibited cellular growth in the hepatocellular carcinoma cell line, Huh7, whereas the RAGE ligand, high mobility group box 1 protein (HMGB1) increased cellular proliferation. In addition, knockdown of RAGE by siRNA arrested cells in the G1 phase and inhibited DNA synthesis (p < 0.01), while HMGB1 protein decreased the number of cells in the G1 phase and increased the number in the S phase (p < 0.05). Furthermore, quantitative real time RT-PCR (qRT-PCR) and Western Blot results demonstrated that RAGE and HMGB1 positively regulate NF-κB p65 expression in Huh7 cells. These studies suggest that RAGE and RAGE ligands are important targets for therapeutic intervention in hepatocellular carcinoma.     

Hepatoprotective and Antioxidant Effects of Licorice Extract against CCl(4)-Induced Oxidative Damage in Rats

Licorice has been used in Chinese folk medicine for the treatment of various disorders. Licorice has the biological capabilities of detoxication, antioxidation, and antiinfection. In this study, we evaluated the antihepatotoxic effect of licorice aqueous extract (LE) on the carbon tetrachloride (CCl(4))-induced liver injury in a rat model. Hepatic damage, as reveled by histology and the increased activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) activities, and decreased levels of serum total protein (TP), albumin (Alb) and globulin (G) were induced in rats by an administration of CCl(4) at 3 mL/kg b.w. (1:1 in groundnut oil). Licorice extract significantly inhibited the elevated AST, ALP and ALT activities and the decreased TP, Alb and G levels caused by CCl(4) intoxication. It also enhanced liver super oxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), Glutathione S-transferase (GST) activities and glutathione (GSH) level, reduced malondialdehyde (MDA) level. Licorice extract still markedly reverses the increased liver hydroxyproline and serum TNF-α levels induced by CCl(4) intoxication. The data of this study support a chemopreventive potential of licorice extract against liver oxidative injury.     

Iron at the Interface of Hepatocellular Carcinoma

Cancer incidence and mortality are rapidly growing, with liver cancer being the sixth most diagnosed cancer worldwide and the third leading cause of cancer death in 2020. A number of risk factors have been identified that trigger the progression to hepatocellular carcinoma. In this review, we focus on iron as a potential risk factor for liver carcinogenesis. Molecules involved in the regulation of iron metabolism are often upregulated in cancer cells, in order to provide a supply of this essential trace element for all stages of tumor development, survival, proliferation, and metastasis. Thus, cellular and systemic iron levels must be tightly regulated to prevent or delay liver cancer progression. Disorders associated with dysregulated iron metabolism are characterized with increased susceptibility to hepatocellular carcinoma. This review discusses the association of iron with metabolic disorders such as hereditary hemochromatosis, non-alcoholic fatty liver disease, obesity, and type 2 diabetes, in the background of hepatocellular carcinoma.     

金黄葡萄球菌肠毒素C2对小鼠移植瘤的抑制作用

目的采用小鼠移植瘤模型,对金黄葡萄球菌肠毒素C2的抗肿瘤作用进行研究,以进一步揭示超抗原在肿瘤治疗方面的意义。方法从金葡菌发酵液中提纯SEC2蛋白,并经SDS-PAGE及测序分析;构建小鼠S180肉瘤和Lewis肺癌移植瘤模型,分别腹腔注射高、中、低剂量(800、400、200 ng/kg)的SEC2,连续给药10 d,同时以环磷酰胺为阳性对照,生理盐水为阴性对照。于给药后第11天处死小鼠,将肿瘤组织分离并称重,比较SEC2对S180肉瘤及Lewis肺癌移植瘤的抑瘤效果。结果在相对分子质量约30 000处可见目的条带,与理论值相符,N-未端氨基酸测序与文献报道一致;SEC2对两种移植瘤均产生较明显抑制作用,高、中、低剂量SEC2对S180肉瘤的抑瘤率分别达到50.60%、31.81%和19.38%,对Lewis肺癌的抑瘤率分别达到55.62%、45.70%和37.78%。结论从动物水平上确认了SEC2的抑瘤效果,为进一步开展超抗原抗肿瘤研究奠定了基础。     

Heat Shock Protein 60 Restricts Release of Mitochondrial dsRNA to Suppress Hepatic Inflammation and Ameliorate Non-Alcoholic Fatty Liver Disease in Mice

Non-alcoholic fatty liver disease (NAFLD), the most common cause of chronic liver disease, consists of fat deposited (steatosis) in the liver due to causes besides excessive alcohol use. The folding activity of heat shock protein 60 (HSP60) has been shown to protect mitochondria from proteotoxicity under various types of stress. In this study, we investigated whether HSP60 could ameliorate experimental high-fat diet (HFD)-induced obesity and hepatitis and explored the potential mechanism in mice. The results uncovered that HSP60 gain not only alleviated HFD-induced body weight gain, fat accumulation, and hepatocellular steatosis, but also glucose tolerance and insulin resistance according to intraperitoneal glucose tolerance testing and insulin tolerance testing in HSP60 transgenic (HSP60Tg) compared to wild-type (WT) mice by HFD. Furthermore, overexpression of HSP60 in the HFD group resulted in inhibited release of mitochondrial dsRNA (mt-dsRNA) compared to WT mice. In addition, overexpression of HSP60 also inhibited the activation of toll-like receptor 3 (TLR3), melanoma differentiation-associated gene 5 (MDA5), and phosphorylated-interferon regulatory factor 3 (p-IRF3), as well as inflammatory biomarkers such as mRNA of il-1β and il-6 expression in the liver in response to HFD. The in vitro study also confirmed that the addition of HSP-60 mimics in HepG2 cells led to upregulated expression level of HSP60 and restricted release of mt-dsRNA, as well as downregulated expression levels of TLR3, MDA5, and pIRF3. This study provides novel insight into a hepatoprotective effect, whereby HSP60 inhibits the release of dsRNA to repress the TLR3/MDA5/pIRF3 pathway in the context of NAFLD or hepatic inflammation. Therefore, HSP60 may serve as a possible therapeutic target for improving NAFLD.     

Dickkopf-1 Promotes Angiogenesis and is a Biomarker for Hepatic Stem Cell-like Hepatocellular Carcinoma

Cancer stemness evinces interest owing to the resulting malignancy and poor prognosis. We previously demonstrated that hepatic stem cell-like hepatocellular carcinoma (HpSC-HCC) is associated with high vascular invasion and poor prognosis. Dickkopf-1 (DKK-1), a Wnt signaling regulator, is highly expressed in HpSC-HCC. Here, we assessed the diagnostic and prognostic potential of serum DKK-1. Its levels were significantly higher in 391 patients with HCC compared with 205 patients with chronic liver disease. Receiver operating characteristic curve analysis revealed the optimal cutoff value of DKK-1 to diagnose HCC and predict the 3-year survival as 262.2 and 365.9 pg/mL, respectively. HCC patients with high-serum DKK-1 levels showed poor prognosis. We evaluated the effects of anti-DKK-1 antibody treatment on tumor growth in vivo and of recombinant DKK-1 on cell proliferation, invasion, and angiogenesis in vitro. DKK-1 knockdown decreased cancer cell proliferation, migration, and invasion. DKK-1 supplementation promoted angiogenesis in vitro; this effect was abolished by an anti-DKK-1 antibody. Co-injection of the anti-DKK-1 antibody with Huh7 cells inhibited their growth in NOD/SCID mice. Thus, DKK-1 promotes proliferation, migration, and invasion of HCC cells and activates angiogenesis in vascular endothelial cells. DKK-1 is a prognostic biomarker for HCC and a functional molecule for targeted therapy.     

Antioxidant,Analgesic, Anti-Inflammatory,and Hepatoprotective Effects of the Ethanol Extract of Mahonia oiwakensis Stem

The aim of this study was to evaluate pharmacological properties of ethanol extracted from Mahonia oiwakensis Hayata stems (MOS_EtOH). The pharmacological properties included antioxidant, analgesic, anti-inflammatory and hepatoprotective effects. The protoberberine alkaloid content of the MOS_EtOH was analyzed by high-performance liquid chromatography (HPLC). The results revealed that three alkaloids, berberine, palmatine and jatrorrhizine, could be identified. Moreover, the MOS_EtOH exhibited antioxidative activity using the DPPH assay (IC₅₀, 0.743 mg/mL). The DPPH radical scavenging activity of MOS_EtOH was five times higher that that of vitamin C. MOS_EtOH was also found to inhibit pain induced by acetic acid, formalin, and carrageenan inflammation. Treatment with MOS_EtOH (100 and 500 mg/kg) or silymarin (200 mg/kg) decreased the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared with the CCl₄-treated group. Histological evaluation showed that MOS_EtOH reduced the degree of liver injury, including vacuolization, inflammation and necrosis of hepatocytes. The anti-inflammatory and hepatoprotective effect of MOS_EtOH were found to be related to the modulation of antioxidant enzyme activity in the liver and decreases in malondialdehyde (MDA) level and nitric oxide (NO) contents. Our findings suggest that MOS_EtOH has analgesic, anti-inflammatory and hepatoprotective effects. These effects support the use of MOS_EtOH for relieving pain and inflammation in folk medicine.     

Leveraging Blood-Based Diagnostics to Predict Tumor Biology and Extend the Application and Personalization of Radiotherapy in Liver Cancers

While the incidence of primary liver cancers has been increasing worldwide over the last few decades, the mortality has remained consistently high. Most patients present with underlying liver disease and have limited treatment options. In recent years, radiotherapy has emerged as a promising approach for some patients; however, the risk of radiation induced liver disease (RILD) remains a limiting factor for some patients. Thus, the discovery and validation of biomarkers to measure treatment response and toxicity is critical to make progress in personalizing radiotherapy for liver cancers. While tissue biomarkers are optimal, hepatocellular carcinoma (HCC) is typically diagnosed radiographically, making tumor tissue not readily available. Alternatively, blood-based diagnostics may be a more practical option as blood draws are minimally invasive, widely availability and may be performed serially during treatment. Possible blood-based diagnostics include indocyanine green test, plasma or serum levels of HGF or cytokines, circulating blood cells and genomic biomarkers. The albumin–bilirubin (ALBI) score incorporates albumin and bilirubin to subdivide patients with well-compensated underlying liver dysfunction (Child–Pugh score A) into two distinct groups. This review provides an overview of the current knowledge on circulating biomarkers and blood-based scores in patients with malignant liver disease undergoing radiotherapy and outlines potential future directions.     

小鼠多能干细胞对小鼠肝脏电离辐射损伤的作用

目的探讨小鼠多能干细胞(mouse pluripotent stem cells,miPS)对小鼠肝脏电离辐射损伤的作用。方法采用医用电子直线加速器进行单次全身性照射(电子辐射线源为6 MeV,照射总剂量为8 Gy,照射剂量率为1. 0 Gy/min)。辐射组于辐射后12和24 h,经小鼠尾静脉注射生理盐水(200μL/只);治疗组于照射后12和24 h,经尾静脉注射mi PS细胞悬浮液[3×106个/(200μL·只)];对照组小鼠不进行辐射,仅注射生理盐水(200μL/只)。末次注射后1、3、7、14 d,记录小鼠体重、计算肝脏指数,并检测小鼠肝脏中超氧化物歧化酶(superoxide dismutase,SOD)及丙二醛(malondialdehyde,MDA)水平;末次注射后14 d,观察小鼠状态,并采用组织病理学方法观察肝脏病理形态学变化。结果与对照组比较,辐射组小鼠精神状态和食欲状况均不佳,体重显著降低(P <0. 05),肝脏指数差异无统计学意义(P> 0. 05),肝脏中SOD活性显著降低(P <0. 01),MDA水平显著升高(P <0. 05);与辐射组比较,治疗组小鼠体重明显升高(P <0. 05),肝脏指数差异无统计学意义(P> 0. 05),肝脏中SOD活性显著升高(P <0. 05),MDA水平显著降低(P <0. 01)。对照组小鼠肝脏组织无明显病变;辐射组小鼠肝细胞发生明显肿胀及肝细胞索紊乱等明显病理变化;治疗组小鼠肝细胞索排列整齐,肝细胞轻度肿胀,病理变化得到改善。结论 miPS可通过其增殖分化减少小鼠体内氧化应激产生的细胞凋亡,对电离辐射造成的小鼠肝脏损害有明显的修复作用。     

Scenedesmus dimorphus藻渣多糖降血脂与抗氧化作用

对二形栅藻（S. dimorphus）藻渣多糖的降血脂和抗氧化能力进行了研究。实验结果表明：二形栅藻藻渣多糖对大鼠体重、肝脏指数和脾脏指数的增加有一定的抑制作用,并能显著降低高血脂大鼠血清甘油三酯（TG）和MDA的含量,提高SOD酶的活力,但对总胆固醇（TC）、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)调节作用不明显。实验结果证实二形栅藻藻渣多糖对大鼠有显著的降低血脂和抗氧化作用。本实验为二形栅藻藻渣的高值化利用提供参考。