矢车菊素-3-O-葡萄糖苷保护RAW264.7细胞免受过氧化氢诱导的氧化损伤

本研究旨在探究矢车菊素-3-O-葡萄糖苷（cyanidin-3-O-glucoside,C3G）对H2O2诱导RAW264.7细胞氧化损伤的保护作用及其机制。通过噻唑蓝法测定C3G和过氧化氢分别对RAW264.7细胞存活率的影响;采用酶联免疫吸附测定法检测细胞内超氧化物歧化酶（superoxide dismutase,SOD）和谷胱甘肽过氧化物酶（glutathione peroxidase,GSH-Px）活力以及一氧化氮（nitric oxide,NO）和丙二醛（malondialdehyde,MDA）水平;利用2’,7’-二氯荧光素二乙酸酯活性氧荧光探针检测细胞内活性氧（reactive oxygen species,ROS）水平;通过逆转录定量聚合酶链式反应和Western blot法分别测定相关mRNA和蛋白表达水平。结果表明,C3G（6.25～25.00 μmol/L）能显著抑制H2O2诱导RAW264.7细胞活性降低（P＜0.05）。C3G显著降低H2O2诱导RAW264.7细胞内ROS过表达、MDA水平和NO释放（P＜0.05）,显著增加SOD和GSH-Px活力（P＜0.05）。此外,与空白对照相比,400 μmol/L H2O2处理组中,蛋白激酶Mst1/2和Kelch样环氧氯丙烷相关蛋白Keap1的mRNA及蛋白相对表达水平显著上调（P＜0.05）,而细胞中核因子E2相关因子和下游抗氧化酶HO-1的mRNA及蛋白相对表达水平显著下调（P＜0.05）;而采用C3G干预RAW264.7细胞,上述相关mRNA及蛋白的相对表达水平被逆转。结论：C3G对H2O2诱导RAW264.7细胞氧化损伤保护作用,可能与激活Mst/Nrf2信号通路和提高抗氧化酶活性有关。     

Hepatoprotective effect of the root extract of Decalepis hamiltonii against carbon tetrachloride-induced oxidative stress in rats

Decalepis hamiltonii, a climbing shrub, grows in the forests of peninsular India and is consumed for its health promoting properties. The hepatoprotective activity of the aqueous extract of the roots of D. hamiltonii with known antioxidant constituents was studied against carbon tetrachloride (CCl₄)-induced oxidative stress and liver injury in rats. Pretreatment of rats with aqueous extract of the roots of D. hamiltonii, single (50, 100 and 200 mg/kg b.w.) and multiple doses (50 and 100 mg/kg b.w. for 7 days) significantly prevented the CCl₄ (1 ml/kg b.w.) induced hepatic damage as indicated by the serum marker enzymes (AST, ALT, ALP, and LDH). Parallel to these changes, the root extract also prevented CCl₄-induced oxidative stress in the rat liver by inhibiting lipid peroxidation and protein carbonylation, and restoring the levels of antioxidant enzymes (SOD, CAT, GPx, GR, and GST) and glutathione. The biochemical changes were consistent with histopathological observations suggesting marked hepatoprotective effect of the root extract in a dose dependent manner. Protective effect of the aqueous extract of the roots of D. hamiltonii against CCl₄-induced acute hepatotoxicity could be attributed to the antioxidant constituents.     

嗜酸乳杆菌胞外蛋白调控MAPK和PI3K-AKT信号途径关键蛋白活化水平

探讨并揭示嗜酸乳杆菌(Lactobacillus acidophilus)CICC6005分泌的相关蛋白质促进肠道健康及分子机制具有重要研究价值。本实验在确定了L.acidophilus CICC6005分泌的胞外蛋白抑制HT-29结肠癌细胞增殖的基础上,进一步探讨67 ku和37 ku的胞外蛋白通过何种途径发挥抑制结肠癌细胞增殖。研究以HT-29细胞作为靶细胞,用丝裂原激活的蛋白激酶(mitogen activated protein kinase,MAPK)和磷脂酰肌醇-3激酶-丝氨酸/苏氨酸蛋白激酶(phosphatidylinositol 3-kinase-protein kinase B,PI3K-AKT)信号通路为考察对象,以Western Blotting为手段,分析两个通路中关键的靶点蛋白p38、c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)、胞外信号调节激酶(extracellular signal-regulated kinase,ERK)、磷酸化p38(phosphorylated p38,p-p38)、磷酸化c-Jun氨基末端激酶(phosphorylated c-Jun N-terminal kinase,p-JNK)、磷酸化的细胞外信号调节蛋白激酶(phosphorylated extracellular signal-regulated kinase,p-ERK)、磷酸化蛋白激酶B(phosphorylated AKT,p-AKT)、PI3K的表达水平,以探讨并阐述源于L.acidophilus CICC6005胞外蛋白调控结肠癌细胞增殖状况的分子机制。结果表明,不同质量浓度的67 ku和37 ku胞外蛋白分别作用HT-29细胞一定时间后,两种胞外蛋白均具有下调两个信号通路途径中p-ERK1/2、p-p38、p-AKT、PI3K蛋白的表达,且存在浓度依赖关系;但对p-JNK、ERK1/2、p38、JNK蛋白的表达没有影响。因此,源于L.acidophilus CICC6005分泌的37 ku和67 ku胞外蛋白表现出显著的抑制HT-29细胞增殖的功能,其机制可能与调控MAPK和PI3K-AKT两个信号通路中几个关键的靶点蛋白的活化水平相关。该研究结果提示,食用嗜酸乳杆菌其分泌的胞外蛋白质将达到维护肠道健康的目标。     

Protective effect of HV-P411, an herbal mixture,on carbon tetrachloride-induced liver fibrosis

This study was performed to examine the anti-fibrotic activity of HV-P411, an herbal mixture of seeds of Vitis vinifera, Schisandra chinensis and Taraxacum officinale extract, against carbon tetrachloride (CCl₄)-induced liver fibrosis. Hepatic fibrosis was induced by intraperitoneal injection of CCl₄ (0.5 ml/kg, twice weekly) for 8 weeks. Rats were treated orally with HV-P411 at 50, 100, 200, and 400 mg/kg once a day. After chronic exposure to CCl₄, the levels of hydroxyproline were markedly increased; these were significantly reduced by HV-P411 at all dose levels. The level of serum aminotransferases and lipid peroxidation were increased after the CCl₄ treatment, while reduced glutathione was decreased. These changes were attenuated by HV-P411. In addition, HV-P411 attenuated CCl₄-induced raised serum concentration of transforming growth factor-β1, and the levels of matrix metalloprotease-2 and tissue inhibitor of metalloprotease-1 mRNAs. Our results suggest that HV-P411 may prevent liver fibrosis by modulating fibrogenesis and fibrolysis.     

Characterisation of polysaccharides from green tea of Huangshan Maofeng with antioxidant and hepatoprotective effects

This study was to examine the hepatoprotective effects of polysaccharides from green tea of Huangshan Maofeng (HMTP) against CCl₄-induced oxidative damage in mice. HMTP is an acidic heteropolysaccharide with galactose (35.0%, mol.%), arabinose (28.9%) and galacturonic acid (11.3%) being the main monosaccharide components. HMTP (400 and 800 mg/kg·bw) administered orally daily for 14 days before CCl₄ administration significantly reduced the impact of CCl₄ toxicity on the serum markers of liver damage, alanine aminotransferase, aspartate aminotransferase, total-cholesterol and triglycerides. This method of HMTP administration also markedly restrained hepatic lipid peroxidation formation of malondialdehyde and 15-F_2t isoprostanes, and elevated the antioxidant levels of hepatic glutathione and superoxide dismutase. These results together with liver histopathology indicated that HMTP exhibited hepatoprotection against CCl₄-induced injury, which was found to be comparable to that of biphenyldicarboxylate. The hepatoprotective effects of HMTP may be due to both the inhibition of lipid peroxidation and the increase of antioxidant activity.     

Anti-inflammatory effects of Punica granatum Linne in vitro and in vivo

Inflammation can cause various physical dysfunctions. Punica granatum Linne (pomegranate), a high phenolic content fruit, is widely used as an antipyretic analgesic in Chinese culture. Pomegranate has shown potential nitric oxide (NO) inhibition in LPS-induced RAW 264.7 macrophage cells. Moreover, pomegranate (100 mg/kg) significantly decreased carrageenan-induced mice paw edema for 1, 3, 4, and 5 h. Therefore, column chromatography combined with in vitro bioassay-guided fractionation was used to isolate the active anti-inflammatory components from the pomegranate. Punicalagin (1), punicalin (2), strictinin A (3), and granatin B (4) were obtained with yields of 0.093%, 0.015%, 0.003%, and 0.013%, respectively. All these hydrolysable tannins inhibited NO production and iNOS expression in RAW 264.7 cells. Among them, 4 showed the strongest iNOS and COX-2 inhibitory effects, and exhibited these effects in the inhibition of paw swelling and the PGE₂ level in carrageenan-induced mice. Taken together, we suggest that 4 could be used as a standard marker for the anti-inflammatory effect of pomegranate.     

Cyanidin-3-glucoside ameliorates CCl4-induced liver injury in mice

The protective effect of cyanidin-3-glucoside (C3G) against carbon tetrachloride (CCl₄)-induced liver injury in mice was investigated. Administration of C3G attenuated the levels of serum aspartate aminotransferase, alanine aminotransferase, and liver lipid peroxidation in CCl₄-treated mice. Histopathological examination of mouse livers showed that C3G reduced the incidence of liver lesions induced by CCl₄. Moreover, C3G prevented DNA damage and decreased the protein levels of γ-H2AX in CCl₄-treated mouse livers. C3G also increased the activity of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, which were decreased due to CCl₄ administration in CCl₄-treated mouse livers. C3G inhibited the expression levels of IL-6 and iNOS in CCl₄-treated mice. C3G apparently protects the liver from CCl₄-induced hepatic damage through antioxidant and anti-inflammatory mechanisms.     

美味牛肝菌多糖对急性肝损伤小鼠的保肝作用

用不同剂量的美味牛肝菌多糖(Boletus edulis polysaccharides,BEP)给予小鼠灌胃连续30d后,按10mL/kg剂量腹腔注射含体积分数0.2%CCl4的花生油溶液,建立CCl4诱导小鼠肝损伤模型。测定肝脏指数、肝脏重量、血清谷丙转氨酶(ALT)、谷草转氨酶(AST),以及肝组织中超氧化物岐化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)及还原型谷胱甘肽(GSH)水平,并进一步观察肝脏组织病理学变化。结果表明:BEP能显著抑制CCl4急性肝损伤小鼠肝脏指数、血清ALT、AST水平以及肝脏MDA含量的升高,提高肝脏GSH-Px、SOD及GSH活性,其中800 mg/(kg BW獉d)剂量水平效果最佳,BEP对CCl4急性肝损伤小鼠有一定的保护作用。     

Enzymatic extracts from edible red algae, <Emphasis Type="Italic">Porphyra tenera</Emphasis>, and their antioxidant,anti-acetylcholinesterase,and anti-inflammatory activities

Enzymatic extracts from Porphyra tenera were prepared using 4 proteases (Protamex, Neutrase, Flavourzyme, and Alcalase) and 7 carbohydrases (AMG, Celluclast, Dextrozyme, Maltogenase, Termamyl, Promozyme, and Viscozyme), and biological activities of the enzymatic extracts from P. tenera were determined as antioxidant, anti-acetylcholinestrase (AChE), and anti-inflammation. The Alcalase and Maltogenase extracts showed higher 1,1-diphenyl-2-picrylhydrozyl (DPPH) scavenging activities compared to the other extracts. At the 2.5 mg/mL, 94.38% (Alacalase extracts), and 80.13% (Maltogenase extracts) scavenging capacities were observed. The Alcalase and Maltogenase extracts were also showed strong reducing power, ferrous ion chelating, and hydrogen peroxide (H2O2) scavenging capacities. In addition, 2 enzymatic extracts effectively protected hydroxyl radical-induced DNA damage. In the case of AChE inhibition, the Flavourzyme (99.32% inhibition) and Viscozyme extracts (82.68% inhibition) were observed. All enzymatic extracts showed no cytotoxicity in RAW264.7 macrophages, and all enzymatic extracts effectively inhibited lipopolysaccharides (LPS)-induced nitric oxide (NO) production in RAW264.7 macrophages. These results suggest that the enzymatic extracts from P. tenera would be useful as an ingredient for functional foods.     

Effects of isomerisation and oxidation on the immunomodulatory activity of chlorogenic acid in RAW264.7 macrophages

Chlorogenic acid (CA) is one of the major polyphenols in fruit that contributes to most bioactivities. However, it is susceptible to isomerisation and oxidation in processing and thus displays varied bioactivity. This study aimed to evaluate the isomerisation and oxidation effects of CA on the potential immunomodulatory activity in RAW264.7 macrophages through the NF-E2-related factor-2 (Nrf2) and nuclear factor-kappa B (NF-κB) signalling pathways. The results showed that isomerisation significantly affected the immunomodulation of CA by reducing Nrf2 and increasing NF-κB nuclear translocation. The oxidation of CA weakened the effect of immune regulation in macrophages through impacts on the nucleic translocation of Nrf2 and NF-κB, cellular reactive oxygen species (ROS) accumulation, antioxidant enzyme (superoxide dismutase, SOD) activity and cytokine expression. Consequently, isomerisation and oxidation remarkably affect the immunomodulation of CA via the Nrf2 and NF-κB pathways.     

Polygonum viviparum L. inhibits the lipopolysaccharide‐induced inflammatory response in RAW264.7 macrophages through haem oxygenase‐1 induction and activation of the Nrf2 pathway

BACKGROUND: Polygonum viviparum L. (PV) is a member of the family Polygonaceae and is widely distributed in high‐elevation areas. It is used as a folk remedy to treat inflammation‐related diseases. This study was focused on the anti‐inflammatory response of PV against lipopolysaccharide (LPS)‐induced inflammation in RAW264.7 macrophages. RESULTS: Treatment with PV did not cause cytotoxicity at 0–50 µg mL^?1 in RAW264.7 macrophages, and the IC₅₀ value was 270 µg mL^?1. PV inhibited LPS‐stimulated nitric oxide (NO), prostaglandin (PG)E₂, interleukin (IL)‐1β and tumour necrosis factor (TNF)‐α release and inducible NO synthase (iNOS) and cyclooxygenase (COX)‐2 protein expression. In addition, PV suppressed the LPS‐induced p65 expression of nuclear factor (NF)‐κB, which is associated with the inhibition of IκB‐α degradation. These results suggest that, among mechanisms of the anti‐inflammatory response, PV inhibits the production of NO and these cytokines by down‐regulating iNOS and COX‐2 gene expression. Furthermore, PV can induce haem oxygenase (HO)‐1 protein expression through nuclear factor E2‐related factor 2 (Nrf2) activation. A specific inhibitor of HO‐1, zinc(II) protoporphyrin IX, inhibited the suppression of iNOS and COX‐2 expression by PV. CONCLUSION: These results suggest that PV possesses anti‐inflammatory actions in macrophages and works through a novel mechanism involving Nrf2 actions and HO‐1. Thus PV could be considered for application as a potential therapeutic approach for inflammation‐associated disorders. © 2012 Society of Chemical Industry     

Hepatoprotective effect of 2,3-dehydrosilybin on carbon tetrachloride-induced liver injury in rats

The aim of this study was to investigate the protective effect of 2,3-dehydrosilybin (DHS) against carbon tetrachloride (CCl₄)-induced liver injury in rats. Administration of DHS significantly attenuated the levels of serum aspartate aminotransferase, alanine aminotransferase, and liver lipid peroxidation in CCl₄-treated rats. Moreover, we showed that DHS prevented DNA damage and decreased the protein levels of γ-H2AX, which is a specific DNA damage marker, in CCl₄-treated rat livers. DHS also markedly increased the activity of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase in CCl₄-treated rat livers. Furthermore, we found that DHS significantly inhibited the production of serum nitric oxide as well as the levels of serum IL-6, IFN-γ, and TNF-α in CCl₄-treated rats. Additionally, DHS significantly suppressed iNOS expression on the protein levels in CCl₄-treated rat livers. Collectively, the present study suggests that DHS protects the liver from CCl₄-induced hepatic damage via antioxidant and anti-inflammatory mechanisms.     

Yerba-mate (Ilex paraguariensis) extract prevents ethanol-induced liver injury in rats

Ethanol metabolism-associated oxidative stress contributes to the pathogenesis of alcoholic liver disease. We examined the effect of a Mate tea extract on ethanol-induced liver injury in vitro and in vivo models. Isolated hepatocytes were incubated with ethanol. An extract of Yerba-Mate tea (EMT) was added to the cultures simultaneously with ethanol. EMT treatment suppressed the ethanol-induced increase in cell death by inhibiting cytochrome p450 2E1 (CYP2E1) activity, which is related to the production of reactive oxygen species. Furthermore, we examined the effects of EMT on serum transaminase activity, and the progression of liver fibrosis in rats treated with ethanol and CCl₄. Rats were fed a diet that included 0.005% or 0.02% EMT or no EMT. For a period of 3 weeks, the animals were provided drinking water containing 5% ethanol and were also treated with carbon tetrachloride (CCl₄) (0.1 ml/kg of body weight). EMT treatment suppressed plasma ALT and AST activities in the ethanol- and CCl₄-treated rats. EMT treatment also decreased CYP2E1 expression and increased ADH expression in the ethanol- and CCl₄-treated rats. EMT treatment fully protected the rats against ethanol- and CCl₄-induced liver injury. These results suggest that EMT may serve as a candidate for preventing ethanol-induced liver injury.     

Protective effect of antrosterol from Antrodia camphorata submerged whole broth against carbon tetrachloride-induced acute liver injury in mice

The hepatoprotective potential of antrosterol (ergostatrien-3β-ol, ST1) from Antrodia camphorata (AC) against carbon tetrachloride (CCl₄)-induced liver damage was evaluated in preventive models in mice. Pretreatment with ST1 markedly prevented the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and liver lipid peroxides in CCl₄-treated mice. The activities of antioxidant enzymes [catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)] were significantly increased after treatment with CCl₄invivo. In addition, ST1 decreased the level of nitric oxide (NO) production and tumour necrosis factor-alpha (TNF-α) in CCl₄-treated mice. In this study, these results pointed out that ST1 can inhibit lipid peroxidation, enhance the activities of antioxidant enzymes, decreases the TNF-α level, nitric oxide production and inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) expressions. Therefore, it was speculated that ST1 protects mice from liver damage through their anti-inflammation capacity.     

The in vivo antioxidant and antifibrotic properties of green tea (Camellia sinensis,Theaceae)

The in vivo antioxidant and antifibrotic properties of green tea (Camellia sinensis, Theaceae) were investigated with a study of carbon tetrachloride (CCl₄)-induced oxidative stress and hepatic fibrosis in male ICR mice. Oral administration of green tea extract at doses of 125, 625 and 1250 mg/kg for 8 weeks significantly reduced (p < 0.05) the levels of thiobarbituric acid-reactive substances (TBARS) and protein carbonyls in the liver by at least 28% compared with that was induced by CCl₄ (1 mL/kg) in mice. Moreover, green tea extract administration significantly increased (p < 0.05) the activities of catalase, glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) in the liver. Our study found that oral administration of green tea extract prevented CCl₄-induced hepatic fibrosis, as evidenced by a decreased hydroxyproline level in the liver and a reduced incidence of hepatic fibrosis by histological observations. These results indicate that green tea exhibits potent protective effects against CCl₄-induced oxidative stress and hepatic fibrosis in mice by inhibiting oxidative damage and increasing antioxidant enzyme activities.     

Hepatoprotective effects of sea buckthorn (Hippophae rhamnoides L.) against carbon tetrachloride induced liver injury in rats

BACKGROUND: Liver injuries induced by carbon tetrachloride are the best‐characterized system of xenobiotic‐induced hepatotoxicity and commonly used model for the screening of hepatoprotective activities of drugs. The present study evaluates the hepatoprotective activity of sea buckthorn (Hippophae rhamnoides L.), family Elaeagnaceae, on carbon tetrachloride (CCl₄)‐induced liver injury in male albino rats. The study was performed on Sprague–Dawley male albino rats weighing about 180–200 g. The animals were pretreated with three different doses of leaf extract (50, 100 and 200 mg kg^?1 body weight) for 5 days. Hepatotoxicity was induced by single oral administration of 1.5 mL CCl₄ kg^?1 body weight on the fifth day. The animals were then sacrificed and assessed for various biochemical parameters. RESULTS: Administration of CCl₄ significantly enhanced glutamate oxaloacetate transferase (GOT), glutamate pyruvate transferase (GPT), alkaline phosphatase (ALP) and bilirubin, and decreased total protein levels in the serum. Treatment with CCl₄ also significantly decreased reduced glutathione (GSH), and decreased glutathione peroxidase and superoxide dismutase activity. CCl₄ treatment also caused a significant increase in hepatic lipid peroxidation as assessed by malondialdehyde (MDA) levels in the tissue. Pretreatment of leaf extract at a concentration of 100 and 200 mg kg^?1 body weight significantly (P < 0.05) protected the animals from CCl₄‐induced liver injury. The extract significantly restricted the CCl₄‐induced increase of GOT, GPT, ALP and bilirubin and better maintained protein levels in the serum. Further, it also enhanced GSH and decreased MDA levels. CONCLUSION: The results show that sea buckthorn leaf extract has significant hepatoprotective effects which might be due to its antioxidant activity and can be developed as a nutraceutical or food supplement against liver diseases. Copyright © 2008 Society of Chemical Industry     

Structural characterisation and immunomodulatory effects of polysaccharides isolated from Dendrobium aphyllum

A crude polysaccharide extract of Dendrobium aphyllum (cDAP, yield 38.15 ± 0.20%) was generated. The D. aphyllum polysaccharide (DAP, M_w 471.586 kDa), purified by DEAE‐Sepharose and Sephadex‐G200 Fast Flow, was composed of mannose (71.3%) and glucose (28.7%), according to GC–MS analysis. Its backbone was composed of β‐d ‐mannopyranose and β‐d ‐glucopyranose residues, as revealed by infrared spectroscopic analysis. Its glycosidic bond was mainly 1, 4‐linked, and the O‐acetyl groups were mainly linked to mannose residues, according to periodate oxidation and Smith degradation analysis. The DAP units polymerised into a filiform‐shaped spatial pattern, as characterised by atomic force microscopy and scanning electron microscopy. DAP treatment enhanced cytokine secretion (nitric oxide, interleukin‐6 and tumour necrosis factor‐α) and pinocytic and phagocytic capacities of RAW 264.7 mouse macrophages. The complement receptor 3 and mannose receptor were identified to be the receptors of DAP on RAW 264.7 cells, indicating that the Akt/mTOR/MAPK and IKK/nuclear factor‐?B pathways could be involved in DAP‐activated immunomodulation.     

红松松仁多糖对脂多糖诱导RAW264.7细胞炎症反应的抑制作用

目的:探讨红松松仁多糖PNP40c-1对脂多糖(Lipopolysaccharides,LPS)诱导RAW264.7细胞炎症反应的抑制作用及可能机制。方法:以LPS刺激RAW264.7细胞诱导炎症模型,分别采用MTT法、比色法、酶联免疫法、RT-PCR和Western Blot等方法,比较LPS诱导前后巨噬细胞的细胞活力、吞噬能力、一氧化氮(nitric oxide,NO)/一氧化氮合酶(nitric oxide synthase,iNOS)和细胞因子表达的变化;同时对Nrf2/HO-1信号通路中关键蛋白核因子E2相关因子2(nuclear factor(erythroid-derived 2)-like 2 protein,Nrf2)和血红素氧化酶-1(heme oxygenase-1,HO-1)的mRNA和蛋白表达水平进行研究,以探讨PNP40c-1的具体作用机制。结果:在LPS诱导RAW264.7细胞的炎症反应中,PNP40c-1以剂量依赖性显著提高巨噬细胞的吞噬能力(P<0.05),抑制LPS诱导的NO和iNOS过量表达;PNP40c-1还可通过Nrf2/HO-1信号通路调节炎症因子如肿瘤坏死因子(tumor necrosis factor-α,TNF-α),白介素-1β(interleukin-1β,IL-1β)、白介素-6(IL-6)的分泌,缓解炎症反应。结论:红松松仁多糖PNP40c-1对LPS诱导的炎症反应具有一定的抑制作用,其作用机制与调节Nrf2/HO-1信号通路有关。