血必净注射液对严重烧伤大鼠血清炎症因子影响的实验研究

目的:观察血必净注射液(XBJI)对严重烧伤大鼠血清炎症细胞因子含量的影响。方法:将SD大鼠随机分为模型组、低剂量XBJI组、中剂量XBJI组、高剂量XBJI组,每组24只。制备烧伤大鼠模型并给予相应药物,1次/d,连续给药7 d。观察各组动物创面愈合情况,并于烧伤后第1、3、7 d分别收集每组大鼠血清,采用双抗体夹心酶联免疫吸附试验法(ELISA)检测血清中促炎细胞因子IL-1β、IL-6、IL-8、肿瘤坏死因子-α(TNF-α)和抗炎细胞因子IL-4、IL-10的含量。结果:与模型组比较,XBJI高剂量组第7 d创面愈合率提高(P<0.05);XBJI中、高剂量组血清促炎因子TNF-α、IL-1β、IL-6含量明显下降,以给药后第3 d时下降最为显著;血清抗炎因子IL-4、IL-10含量明显升高。结论:XBJI可通过调节血清炎症细胞因子含量减轻严重烧伤大鼠早期的炎症反应。

Unveiling osteoprotective potential of biologically active naringenin in rats with dexamethasone-induced osteoporosis

Objective To investigate the protective effects of naringenin(NRG)against dexamethasone(DEX)-induced osteoporosis(OP)in rats.Methods Molecular docking of NRG was done with AutoDock Vina 1.2.0 software.Forty-eight female Wistar rats were randomly divided into six groups(n=8 each):normal control(NC),DEX(7 mg/kg,i.m.),NRG-low(NRG-L;25 mg/kg,i.g.),NRG-medium(NRG-M;50 mg/kg,i.g.),NRG-high(NRG-H;100 mg/kg,i.g.),and alendronate(ALN;0.25 mg/d,i.g.)groups.OP was induced by administering DEX once a week for five weeks in all groups except NC group.Begining in the third week after the initial DEX administration,the rats in NRG-L,NRG-M,NRG-H,and ALN groups received the corresponding treatments daily for three weeks,while NC and DEX groups received no additional treatment.Serum samples were collected at the end of the experiment for biochemical,bone turnover,antioxidant,lipid profile,and inflammatory cytokine analyses.Femur bones underwent physical parameter testing and histopathological examination.Results The molecular docking results illustrated that NRG docked with calcitonin(CT),lowdensity lipoprotein(LDL),bone morphogenetic protein(BMP),vascular endothelial growth factor(VEGF)receptor,forkhead transcription factors,and osteoprogenitor cells showed good binding energy.In rats administered with 25,50,and 100 mg/kg NRG,there was a significant enhancement in serum biochemical indices,characterized by a reduction in tartrate-resistant acid phosphatase(TRAP),parathyroid hormone(PTH),and an elevation in osteocalcin(OC)and CT levels(P<0.05,P<0.01,and P<0.001,respectively).Despite no significant changes in thickness,weight,and length(P>0.05),there was a marked increase in bone mineral density(BMD)(P<0.01,P<0.001,and P<0.001,respectively).Antioxidant enzyme markers showed significant upregulation,with higher glutathione,superoxide dismutase,and catalase,and a concurrent decrease in malondialdehyde(MDA)(P<0.05,P<0.01,and P<0.001,respectively).The lipid profile also improved significantly,with lower cholesterol(CH),triglycerides(TG),and low-density lipoprotein(LDL)levels,and an increase in high-density lipoprotein(HDL)level(P<0.05,P<0.01,and P<0.001,respectively).Inflammatory cytokine levels were reduced,as evidenced by decreases in tumor necrosis factor(TNF),interleukin(IL)-6,and IL-1β(P<0.05,P<0.01,and P<0.001,respectively).Furthermore,histological alterations revealed obvious improvements,and the body weight of rats treated with NRG showed an increase compared with DEX group.Conclusion These findings imply that NRG exhibited a protective effect against DEX-induced OP in rats as it promotes the bone formation process by increasing the number of bone turnover markers including OC and CT,and restoring of antioxidant status,lipid metabolism,and inflammatory markers.

Role of the endothelium in inflammatory bowel diseases

Inflammatory bowel diseases(IBD) are a complex group of diseases involving alterations in mucosal immunity and gastrointestinal physiology during both initiation and progressive phases of the disease.At the core of these alterations are endothelial cells,whose continual adjustments in structure and function coordinate vascular supply,immune cell emigration,and regulation of the tissue environment.Expansion of the endothelium in IBD(angiogenesis),mediated by inflammatory growth factors,cytokines and chemokines,is a hallmark of active gut disease and is closely related to disease severity.The endothelium in newly formed or inflamed vessels differs from that in normal vessels in the production of and response to inflammatory cytokines,growth factors,and adhesion molecules,altering coagulant capacity,barrier function and blood cell recruitment in injury.This review examines the roles of the endothelium in the initiation and propagation of IBD pathology and distinctive features of the intestinal endothelium contributing to these conditions.

A rabbit model of pediatric nonalcoholic steatohepatitis: The role of adiponectin

AIM： To create a rabbit model of pediatric nonalcoholic steatohepatitis （NASH） and to evaluate the role of adiponectin in the process. METHODS： Thirty-two specific pathogen-free male New Zealand rabbits were divided randomly into three groups： （1） the normal control group （n = 10） was fed with standard diet for 12 wk; （2） the model group A （n = 11）; and （3） model group B （n = 11） were fed with a highfat diet （standard diet ＋ 10% lard ＋ 2% cholesterol） for 8 and 12 wk, respectively. Hepatic histological changes were observed and biochemical parameters as well as serum levels of adiponectin, interleukin （IL）-6, IL-10 and tumor necrosis factor （TNF）-α were measured. RESULTS： Typical histological hepatic lesions of NASH were observed in both model groups described as liver steatosis, liver inflammatory infiltration, cytologic ballooning, perisinusoidal fibrosis and overall fibrosis. Compared with the normal control group, there were significant increases in model groups A and B in weight gain （1097.2 ± 72.3, 1360.5± 107.6 vs 928.0 ±58.1, P 〈 0.05, P 〈 0.01）, liver weight （93.81±6.64, 104.6±4.42 vs 54.4±1.71, P 〈 0.01）, Lg （ALT） （1.9±0.29, 1.84± 0.28 vs 1.60±0.17, P 〈 0.01）, and Lg （TG） （1.03 ±0.24, 1.16 ±0.33 vs 0.00 ±0.16, P 〈 0.01）. Weight gain was much more in model group B than in model group A （1360.5± 107.6 vs 1097.2 ±72.3, P 〈 0.05）. But, there was no significant difference between the two groups concerning the other indexes. Pro-inflammatory cytokines （IL-6 and TNF-α） increased in model group B compared with that of control and model group A （IL-6：1.86±0.21 vs 1.41 ±0.33, 1.38± 0.42, P 〈 0.01; TNF-α： 1.18±0.07 vs 0.66 ±0.08, 0.86 ±0.43, P 〈 0.01, P 〈 0.05）, whereas serum adiponectin and IL-10 decreased in model groups compared with that in the control （adiponectin： A： 21.87±4.84 and B： 21.48 ±4.60 vs 27.36 ±7.29, P 〈 0.05. IL-10： A： 1.72± 0.38 and B： 1.83 ±0.39 vs 2.26±0.24, P 〈 0.01）. Lg （TC） and the degree of liver fatty infiltration was an independent determinant of serum adiponectin level analyzed by stepwise multiple regressions, resulting in 29.4% of variances. CONCLUSION： This rabbit model produces the key features of pediatric NASH and may provide a realistic model for future studies. Adiponectin level partially reflects the severity of liver steatosis, but not the degree of liver inflammation.

Effect of 5-FU on modulation of disarrangement of immune-associated cytokines in experimental acute pancreatitis

AIM： To investigate the effects of 5-Fluorouracil （5-FU） on modulation of pro-inflammatory and anti-inflammatory cytokines in acute pancreatitis and the mechanism of it in the treatment of acute pancreatitis. METHODS： Male Sprague Dawley rats were assigned to 3 Groups： Group A, sham operated rats as controls （n = 7）; Group B, acute pancreatitis induced by ductal injection with 5% sodium cholate at a volume of 1.0 mL/kg without any other treatment; Group C, after the pancreatitis was induced as in Group B, the rats were injected intravenously with 5-FU 40 mg/kg. The animals in Groups B and C were killed at 2, 6 and 24 h after operation （n = 7）, and blood samples were taken for measurement of tumor necrosis factor-α （TNF-α）, interleukin-1 （IL-1）, interleukin-6 （IL-6） （by bioassay）, and interleukin-10 （IL-10）, transforming growth factor-β （TGF-β） （by ELISA）. The wet weight of pancreatic tissue, serum amylase levels and white blood cells were also measured. RESULTS： Four rats in Group B and one in Group C died after pancreatitis was induced. Both pro-inflammatory cytokines （TNF-α, IL-1, IL-6） at the 2 and 6 h period and the anti-inflammatory cytokines （IL-10, TGF-β） at 24 h increased significantly （P 〈 0.05） in rats of Group B. After treatment with 5-FU, TNF-α, IL-1, and IL-6 in serum of rats of Group C were inhibited at 2 and 6 h after operation （P 〈 0.05）, and IL-IO, TGF-13 were inhibited at 24 h compared to Group B （P 〈 0.05）. Obvious improvements in the severity of the acute pancreatitis, including the amylase levels, wet weight of pancreatic tissue and neutrophil counts, were also observed after treatment with 5-FU. CONCLUSION： 5-FU is an anti-metabolic and immunosuppressive agent which can minimize the abnormal immune o/tokine response and relieve the pathophysiological disorders associated with experimental acute pancreatitis.

Attenuation of gastric mucosal inflammation induced by aspirin through activation of A_(2A) adenosine receptor in rats

AIM： To determine whether a specific adenosine A2A receptor agonist （ATL-146e） can ameliorate aspirin-induced gastric mucosal lesions in rats, and reduce neutrophil accumulation and production of pro-inflammatory cytokines. METHODS： Gastric lesions were produced by oral gavage of aspirin （200 mg/kg） and HCI （0.15 mol/L, 8.0 mL/kg）. 4-{3-[6-Amino-9-（5-ethylcarbamoyl-3,4- dihydroxy-tetrahydro-furan-2-yl）-9H-purin-2-yl]-prop-2- ynyl}-cyclohexanecarboxylic acid methyl ester （ATL-146e, 2.5-5μg/kg, IP） was injected 30 min before the administration of aspirin. Tissue myeloperoxidase （MPO） concentration in gastric mucosa was measured as an index of neutrophil infiltration. Gastric mucosal concentrations of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） were determined by ELISA. Also, we examined the effect of ATL-146e on tissue prostaglandin E2 （PGE2） production and gastric secretion. RESULTS： Intragastric administration of aspirin induced multiple hemorrhagic erosions in rat gastric mucosa. The total length of gastric erosions （ulcer index） in control rats was 29.8±7.75 mm and was reduced to 3.8±1.42 mm alter pretreatment with 5.0 g/kg ATL-146e （P〈 0.01）. The gastric contents of MPO and pro-inflammatory cytokines were all increased after the administration of aspirin and reduced to nearly normal levels by ATL-146e. Gastric mucosal PGE2 concentration was not affected by intraperitoneal injection of ATL-146e. CONCLUSION： The specific adenosine A2A receptor agonist, ATL-146e, has potent anti-ulcer effects presumably mediated by its anti-inflammatory properties.

CD74 in antigen presentation,inflammation,and cancers of the gastrointestinal tract

CD74 is a protein whose initial role in antigen presentation was recognized two decades ago. Recent studies have revealed that it has additional functions as a receptor for macrophage migration inhibitory factor and as a receptor for an important human pathogen, Helicobacter pylori （H pylon）. The role of CD74 as a receptor is important because after binding of migration inhibitory factor or H pylori, NF-κB and Erkl/2 activation occurs, along with the induction of proinflammatory cytokine secretion. This review provides an up-to-date account of the functions of CD74 and how it might be involved in inflammation and cancer within the gastrointestinal tract.

Blockage of PPARδ increases the expression of inflammatory factors in 3T3-L1 cells stimulated with TNFα

Objective： To investigate the role of peroxisome proliferator-activated receptors δ （PPARδ） in inflammatory reaction and its possible mechanism in adipocyte. Methods：Lentivirus-mediated RNA interference （RNAi） was used to block the expression of PPARδ in 3T3-L1 cells. In order to induce inflammation in 3T3-L1, cells were stimulated with tumor necrosis factor-α（TNFα, 20 ng/ml） for 4 h. The expression of PPARδ, nuclear factor κB （NFκB） and C reactive protein （CRP） were determined by Western blot analysis. Results：The expression of PPARδ was reduced by 80% after RNAi. Blockage of PPARδ promoted the expression of CRP and NFκB in cells stimulated with TNFα but had no effect on normal cells. Conclusion： PPARδ is involved in inflammatory reaction in adipocyte. Blockage of PPARδ can promote the inflammation mediated by inflammatory factors and increase the expression of NFκB and CRP in 3T3-L1 cells stimulated with TNFα.

Lipopolysaccharide preconditioning induces protection against lipopolysac-charide -induced neurotoxicity in organotypic midbrain slice culture

Objective To identify the protective effect of lipopolysaccharide （LPS） preconditioning against LPS-induced inflammatory damage in dopaminergic neurons of midbrain slice culture and the possible mechanisms. Methods After cultured in vitro for 14 d, the rat organotypic midbrain slices were pretreated with different concentrations （0, 1, 3, 6 or 10 ng/mL） of LPS for 24 h followed by treatment with 100 ng/mL LPS for 72 h. The whole slice viability was detelmined by measurement of the activity of lactic acid dehydrogenase （LDH）. Tyrosine hydroxylase-immunoreactive （TH-IR） neurons and CD 1 1 b/c equivalent-immunoreactive （OX-42-IR） microglia in the slices were observed by immunohistochemical method, and tumor necrosis factor-α （TNF-α levels in the culture media were detected by enzymelinked immunosorbent assays （ELISA）. Results In the slices treated with 100 ng/mL LPS for 72 h, the number of TH-IR neurons reduced from 191± 12 in the control slices to 46±4, and the LDH activity elevated obviously （P 〈 0.01）, along with remarkably increased number of OX-42-IR cells and production of TNF-α （P 〈 0.01）. Preconditioning with 3 or 6 ng/mL LPS attenuated neuron loss （the number of TH-IR neurons increased to 126± 12 and 180± 13, respectively） and markedly reduced LDH levels （P 〈 0.05）, accompanied by significant decreases of OX-42-IR microglia activation and TNF-α production （P 〈 0.05）. Conclusion Low-dose LPS preconditioning could protect dopaminergic neurons against inflammatory damage in rat midbrain slice culture, and inhibition of microglial activation and reduction of the proinflammatory factor TNF-α production may contribute to this protective effect. Further understanding the underlying mechanism of LPS preconditioning may open a new window for treatment of Parkinson＇s disease.

A novel heterodimeric cytokine consisting of IL-17 and IL-17F regulates inflammatory responses

CD4＋ helper T （TH） cells play crucial roles in immune responses. Recently a novel subset of TH cells, termed THIL-17, TH 17 or inflammatory TH （THi）, has been identified as critical mediators of tissue inflammation. These cells produce IL-17 （also called IL-17A） and IL-17F, two most homologous cytokines sharing similar regulations. Here we report that when overexpressed in 293T cells, IL-17 and IL-17F form not only homodimers but also heterodimers, which we name as IL-17A/F. Fully differentiated mouse THi cells also naturally secrete IL-17A/F as well as IL-17 and IL-17F homodimeric cytokines. Recombinant IL-17A/F protein exhibits intermediate levels of potency in inducing IL-6 and KC （CXCL 1） as compared to homodimeric cytokines. IL-17A/F regulation of IL-6 and KC expression is dependent on IL-17RA and TRAF6. Thus, IL-17A/F cytokine represents another mechanism whereby T cells regulate inflammatory responses and may serve as a novel target for treating various immune-mediated diseases.

Value of adipokines in predicting the severity of acute pancreatitis:Comprehensive review

AIM:To analyze the prognostic value of adipokines in predicting the course,complications and fatal outcome of acute pancreatitis(AP).METHODS:We performed the search of PubMed database and the systemic analysis of the literature for both experimental and human studies on prognostic value of adipokines in AP for period 2002-2012.Only the papers that described the use of adipokines for prediction of severity and/or complications of AP were selected for further analysis.Each article had to contain information about the levels of measured adipokines,diagnosis and verification of AP,to specify presence of pancreatic necrosis,organ dysfunction and/or mortality rates.From the very beginning,study was carried out adhering to the PRISMA checklist and flowchart for systemic reviews.To assess quality of all included human studies,the Quality Assessment of Diagnostic Accuracy Studies tool was used.Because of the high heterogeneity between the studies,it was decided to refrain from the statistical processing or meta-analysis of the available data.RESULTS:Nine human and three experimental studies were included into review.In experimental studies significant differences between leptin concentrations at 24 and 48 h in control,acute edematous and acute necrotizing pancreatitis groups were found(P = 0.027 and P < 0.001).In human studies significant differences between leptin and resitin concentrations in control and acute pancreatitis groups were found.1-3 d serum adiponectin threshold of 4.5 μg/mL correctly classified the severity of 81% of patients with AP.This threshold yielded a sensitivity of 70%,specificity 85%,positive predictive value 64%,negative predictive value88%(area under curve 0.75).Resistin and visfatin concentrations differ significantly between mild and severe acute pancreatitis groups,they correlate with severity of disease,need for interventions and outcome.Both adipokines are good markers for parapancreatic necrosis and the cut-off values of 11.9 ng/mL and 1.8 ng/mL respectively predict the high ranges of radiological scores.However,the review revealed that all nine human studies with adipokines are very different in terms of methodology and objectives,so it is difficult to generalize their results.It seems that concentrations of the leptin and resistin increases significantly in patients with acute pancreatitis compared with controls.Serum levels of adiponectin,visfatin and especially resitin(positive correlation with Acute Physiology and Chronic Health Evaluation Ⅱ,Ranson and C-reactive protein) are significantly different in mild acute pancreatitis and severe acute pancreatitis patients,so,they can serve as a markers for the disease severity prediction.Resistin and visfatin can also be used for pancreatic and parapancreatic necrosis prediction,interventions needs and possible,outcome.CONCLUSION:High levels of adipokines could allow for prediction of a severe disease course and outcome even in small pancreatic lesions on computed tomography scans.

The roles of toll-like receptors in carcinogenesis and cancer immunotherapy

Toll-like receptors （TLRs） are probably the most important class of pattern-recognition receptors. Members of the TLR family play key roles in the both innate and adaptive immune responses. Recognition of pathogen-associated molecular patterns （PAMPs） by TLRs, either alone or in heterodimedzation with other TLR or non-TLR receptors, induces the production of signals that are responsible for the activation of genes important for an effective host defense, especially those of proinflammatory cytokines. Thus, TLRs are involved in the development of many pathological conditions including infectious diseases, tissue damage, and cancer especially. In this review, the contribution of TLRs to tumorgenesis is evaluated. We hope to provide new insight into the progression of cancer and more importantly into the potential for TLRs as targets of therapeutics.

Adenosine:An immune modulator of inflammatory bowel diseases

Inflammatory bowel disease(IBD)is a common and lifelong disabling gastrointestinal disease.Emerging treatments are being developed to target inflammatory cytokines which initiate and perpetuate the immune response.Adenosine is an important modulator of inflammation and its anti-inflammatory effects have been well established in humans as well as in animal models.High extracellular adenosine suppresses and resolves chronic inflammation in IBD models.High extracellular adenosine levels could be achieved by enhanced adenosine absorption and increased de novo synthesis.Increased adenosine concentration leads to activation of the A2a receptor on the cell surface of immune and epithelial cells that would be a potential therapeutic target for chronic intestinal inflammation. Adenosine is transported via concentrative nucleoside transporter and equilibrative nucleoside transporter transporters that are localized in apical and basolateral membranes of intestinal epithelial cells,respectively. Increased extracellular adenosine levels activate the A2a receptor,which would reduce cytokines responsible for chronic inflammation.

The therapeutic mechanism of Shenyuan Gan in lipopolysaccharide-induced neuroinflammation in BV2 microglial cells

Objective To study the therapeutic effects of Shenyuan Gan(参远苷,SYG)on the inflammat-ory response in BV2 microglial cells induced by lipopolysaccharide(LPS).Methods The cytotoxicity of SYG to BV2 microglial cells was evaluated using a Cell Counting Kit-8(CCK-8)assay,and the effect of SYG concentrations on LPS-induced BV2 microglial cells was studied.The morphological changes were observed using an optical microscope.The nitric oxide(NO)concentration in cell culture supernatant was determined using Griess re-agent.The expression of cytokines and inflammatory mediators were also measured by an en-zyme-linked immunosorbent assay(ELISA).Western blot analysis was used to determine the levels of inducible NO synthase(iNOS),nuclear factor-kappa B(NF-κB)p65,alpha inhibitor of NF-κB(IκB-α),phosphorylation-IκB-α(p-IκB-α),NOD-like receptor 3(NLRP3),and cas-pase-1 expression.Moreover,the expression of iNOS,NLRP3,and ionized calcium binding adapter molecule 1(Iba1)was also observed using immunofluorescent staining.Results SYG had a low cytotoxic effect on BV2 microglial cells and could significantly decr-ease LPS-induced morphological changes of BV2 microglial cells(P<0.05).ELISA results showed that SYG significantly inhibited the LPS-induced increase in interleukin(IL)-1βand IL-6 in BV2 microglia cells(P<0.05),and Western blot analysis showed that the phosphoryla-tion levels of iNOS,NF-κB p65,and IκB-αas well as NLRP3 and caspase-1 expression were also significantly decreased,and IκB-αexpression was increased after SYG treatment(P<0.05,compared with the LPS-treated group).The immunofluorescence results were consist-ent with the Western blot results,and Iba1 staining indicated that the cell morphology tended to be resting.These results indicate that SYG has a certain inhibitory effect on LPS-induced inflammation in BV2 microglial cells.Conclusion SYG can inhibit LPS-induced release of inflammatory factors in BV2 microglial cells by affecting the phosphorylation levels of NF-κB p65 and IκB-α.SYG is a valuable candid-ate for treating neuroinflammation-related diseases.

Changes of the cytokine profile in inflammatory bowel diseases

Cytokines are indispensable signals of the mucosaassociated immune system for maintaining normal gut homeostasis.An imbalance of their profile in favour of inflammation initiation may lead to disease states,such as that is observed in inflammatory bowel diseases(IBD).Although Crohn's disease(CD) is often described as a prototype of T-helper 1-type diseases,and ulcerative colitis(UC) is traditionally viewed as a T-helper 2-mediated condition,the classic paradigm,which categorises cytokines into pro-and anti-inflammatory groups,has recently been changed.The inflammation regulatory pathways may not be mutually exclusive as individual cytokines can have diverse and even opposing functions in various clinical and immunological settings.None the less there are many common immunological responses in IBD that are mediated by cytokines.Although they regulate and influence the development,course and recurrence of the inflammatory process,the concrete pathogenic role of these small signaling molecules is sometimes not unambiguous in the subtypes of the disease.Our aim is to review the current information about pro-and anti-inflammatory effects of traditionally studied and recently discovered cytokines in the pathogenesis of UC and CD.The better understanding of their production and functional activity may lead to the development of new therapeutic modalities.

Alcohol metabolites and lipopolysaccharide: Roles in the development and/or progression of alcoholic liver disease

The onset of alcoholic liver disease (ALD) is initiated by different cell types in the liver and a number of different factors including: products derived from ethanol-induced inflammation, ethanol metabolites, and the indirect reactions from those metabolites. Ethanol oxidation results in the production of metabolites that have been shown to bind and form protein adducts, and to increase inflammatory, fibrotic and cirrhotic responses. Lipopolysaccharide (LPS) has many deleterious effects and plays a significant role in a number of disease processes by increasing inflammatory cytokine release. In ALD, LPS is thought to be derived from a breakdown in the intestinal wall enabling LPS from resident gut bacterial cell walls to leak into the blood stream. The ability of adducts and LPS to independently stimulate the various cells of the liver provides for a two-hit mechanism by which various biological responses are induced and result in liver injury. Therefore, the purpose of this article is to evaluate the effects of a two-hit combination of ethanol metabolites and LPS on the cells of the liver to increase inflamma-tion and fi brosis, and play a role in the development and/or progression of ALD.

The Role of Inflammation in Breast Cancer and Prostate Cancer

Inflammatory conditions increase the risk of cancer. Strong evidences showed that inflammation contributes to breast cancer and prostate cancer in different ways such as inflammationinduced DNA or RNA damage, overexpression cytokines, chemokines etc. Recent studies have begun to unravel molecular pathways linking inflammation and cancer. Some possible mechanisms by which inflammation can contribute to carcinogenesis have been found. These mechanisms by which inflammation contributes to cancer give broader views of cancer development. These insights are fostering new antiinflammatory therapeutic approaches to cancer development.

Medicinal properties and anti-inflammatory components of Phytolacca(Shanglu)

Phytolacca(Shanglu)is a well-known traditional herbal medi-cine that has been used for thousands of years in China.Phytolacca is also used worldwide in different traditional phyto-medicines and homeopathic preparations.The present work re-viewed advances in the traditional uses,plant origin,chemical constituents,pharmacology,and medicinal properties of Phytolacca.Phytolacca is usually made from the roots of Phytolacca acinosa and P.esculenta,but the invasive plant P.americana(American pokeweed)is also widely used.Different types of medicinal products made with Phytolacca are available,as well as various types of Phytolacca extracts,showing a range of pharmacological activities including antioxidant,anti-inflammat-ory,anti-parasitic,antifungal,anticancer,and insecticidal effects.The marked anti-inflammatory activity of Phytolacca extracts supports its use in treating diseases such as arthritis,nephritis,and rheumatism,as well as in combatting cancer.Several bioact-ive natural products have been identified from Phytolacca,in-cluding glycosylated saponins such as esculentosides and phytolaccosides,as well as a few flavones(cochliophilin A)and phytosterols(α-spinasterol),which contribute to Phytolacca’s anti-inflammatory and/or anticancer effects.A quality evaluation of Phytolacca-based extracts and products is highly recommen-ded;nevertheless,the use of Phytolacca can be encouraged to help regulate cytokine production and combat inflammatory dis-eases.

Effects of interleukin-18 on airway inflammation and the Th1/Th2 cytokine imbalance in guinea pig asthmatic model

In order to investigate the effects of interleukin-18 （IL-18） on airway inflammation and the Th1/Th2 cytokine balance in guinea pig asthmatic model as well as its possible mechanisms, the asthmatic model was established by intraperitoneal injection of ovalbumin （OVA） and aerosol challenges into guinea pigs, and 30 treated animals were randomly divided into three groups of 10 animals in each groups, in which group A served as the asthmatic model, group B as the controls and group C as the group treated with IL-18. The counting and categorization of the inflammatory cells in bronchoalveolar lavage fluid （BALF） were performed by using light microscopy, and the contents of cytokines （ IFN-γ, IL- 2, IL-4 and IL-5） were assayed by means of the ELISA kit. The experimental results showed that the numbers of eosinophils （ESO） in BALF of group A, B and C were （97.70 ± 58.03） × 10^6/L, （11.68 × 9.95） × 10^6/L and （28.62 ± 10.46） × 10^6/L, respectively, in which the number of eosinophils in group A was significantly higher than those of group B and C. Also, the number of neutrophils in BALF of group A was even higher than those in group B and C. In addition, the contents of IFN-7 and IL-2 in group A were lower than those in group B and C, but the contents of IL-4 as well as IL-5 were rather higher than those in group B and C. It is evident from the above observations that IL-18 can effectively inhibit the asthmatic inflammatory cells in BALF with an imbalance of the Thl/Th2 cytokines, thus offer- ing the experimental basis for the clinical application of IL-18 in the prevention and treatment of asthma.

Anti--inflammatory effect of ethyl acetate extract of Sedum aizoon L. in LPS-stimulated RAW 264.7 macrophages and its HPLC fingerprint

Sedum aizoon L.（SA） has been widely used for treatment of various hemorrhages, insomnia, pain and trauma？ however, its anti-inflammatory activity is unknown. In this study, we firstly investigated the anti--inflammatory activity of SA extracts by petroleum ether（PE）, ethyl acetate（EtOAc）, and H2O in LPS-stimulated RAW 264.7 cells. Results showed that the EtOAc extract rich in phenolics and flavonoids significantly inhibited LPS-induced NO, TNF--α, and IL-6 production in RAW 264.7 cells（P0.01）, suggesting that this extract possessed potent anti--inflammatory activity. The phytochemical profile of the effective extract was subsequently analyzed by HPLC fingerprint with 11 standards. The results indicated that gallic acid, protocatechuic acid, p--hydroxybenzoic acid, ethyl gallate, iriflophene, 5,7-dihydroxy chromone, quercitrin, quercetin, luteolin, kaempferol, and isorhamnetin were present in this extract, which might contribute to its anti-inflammatory activity. Thus, the Et -OAc extract of SA showed anti-inflammatory activity and could be used as a potential natural anti--inflammatory agent.