肿瘤细胞“炎化”与NF-κB信号通路的非编码RNA调控

作为转录因子,NF-κB通过转录调节基因表达参与肿瘤的发生进展。诸多研究表明,几乎在所有肿瘤中都存在肿瘤细胞内NF-κB信号通路的持续激活。然而,本来在生理状态下受到严格调控的NF-κB信号通路在肿瘤细胞中如何持续地被激活,其细胞分子生物学机制尚不清楚。现就简要评述非编码RNA(miRNA和lncRNA)对肿瘤细胞内NF-κB炎性通路的调节及其可能的临床转化意义。

Role of microglial polarization in age-related macular degeneration

Microglia,originating from primitive macrophages in the yolk sac,serves as both immune system defenders and regulators of homeostasis.These cells exhibit two primary polarization states:conventionally activated(M1)and alternatively activated(M2).The polarization of microglia plays a crucial role in influencing inflammatory disorders,metabolic imbalances,and neural degeneration.This process is implicated in various aspects of ocular diseases,especially age-related macular degeneration(AMD),including inflammation,oxidative stress and pathological angiogenesis.The distinct functional phenotypes of microglia impact disease progression and prognosis.Thus,regulating the polarization or functional phenotype of microglia at different stages of AMD holds promise for personalized therapeutic approaches.This comprehensive review outlines the involvement of microglia polarization in both physiological and pathological conditions,emphasizing its relevance in AMD.The discussion underscores the potential of polarization as a foundation for personalized treatment strategies for AMD.

Hydration transformation behaviors of CO_(2) and excellent anti-inflammatory activity on RAW 264.7 cell

Skin care products with carbonic acid(H_(2)CO_(3))have gained extensive attention worldwide.However,the conversion of CO_(2) to H_(2)CO_(3) is not stable,and the mechanism of the effect of H_(2)CO_(3) on skin care has not been clearly proved.The hydration-dissolution behaviors of CO_(2) were investigated under different temperature,pH,and pressure conditions.Moreover,based on the phenomenon of CO_(2) hydration transformation,the inflammatory effect of CO_(2) hydrate on macrophages(RAW 264.7)was investigated.The result shows that the increase in temperature weakened the hydration of CO_(2),and the increase in pH and pressure both promoted the water-phase transformation of CO_(2).When pH<6,CO_(2) reacts with water to generate H_(2)CO_(3).When pH was between 6-7,the prompt solution was a mixture of H_(2)CO_(3) and HCO_(3)^(-).When the pH was between 7-9,they mainly generated HCO_(3)^(-).And when pH>9,CO_(2) solubility mainly converts to CO_(3)^(2-).Besides,CO_(2) can inhibit the secretion of inflammatory factors by RAW 264.7 cells by inhibiting the phosphorylation of the p38 protein.CO_(2) hydrate inhibited the expression of pro-inflammatory factors IL-6,TNF-α,and up-regulated the expression of anti-inflammatory factor IL-10.Furthermore,the anti-inflammatory molecular mechanism of CO_(2) hydration inhibited the MAPK signaling pathway by inhibiting the phosphorylation of p38.The hydration-dissolution behavior of CO_(2) was investigated.This work revealed the anti-inflammatory bioeffect of CO_(2) hydrate,providing a theoretical basis and application support for CO_(2) skin care products.

Two-sample Mendelian randomization analysis of causal relationship between eczema and autoimmune diseases

Objective:The causal relationship between eczema and autoimmune diseases has not been previously reported.This study aims to evaluate the causal relationship between eczema and autoimmune diseases.Methods:The two‐sample Mendelian randomization(MR)method was used to assess the causal effect of eczema on autoimmune diseases.Summary data from the Genome-Wide Association Study Catalog(GWAS)were obtained from the Integrative Epidemiology Unit(IEU)database.For eczema and autoimmune diseases,genetic instrument variants(GIVs)were identified according to the significant difference(P<5×10−8).Causal effect estimates were generated using the inverse‐variance weighted(IVW)method.MR Egger,maximum likelihood,MR-PRESSO,and MR-RAPS methods were used for alternative analyses.Sensitivity tests,including heterogeneity,horizontal pleiotropy,and leave-one-out analyses,were performed.Finally,reverse causality was assessed.Results:Genetic susceptibility to eczema was associated with an increased risk of Crohn’s disease(OR=1.444,95%CI 1.199 to 1.738,P<0.001)and ulcerative colitis(OR=1.002,95%CI 1.001 to 1.003,P=0.002).However,no causal relationship was found for the other 6 autoimmune diseases,including systemic lupus erythematosus(SLE)(OR=0.932,P=0.401),bullous pemphigoid(BP)(OR=1.191,P=0.642),vitiligo(OR=1.000,P=0.327),multiple sclerosis(MS)(OR=1.000,P=0.965),ankylosing spondylitis(AS)(OR=1.001,P=0.121),rheumatoid arthritis(RA)(OR=1.000,P=0.460).Additionally,no reverse causal relationship was found between autoimmune diseases and eczema.Conclusion:Eczema is associated with an increased risk of Crohn’s disease and ulcerative colitis.No causal relationship is found between eczema and SLE,MS,AS,RA,BP,or vitiligo.

High Rate of P16 Methylation Associated with Hepatitis B Virus Infection in Hepatocellular Carcinoma

Objective： To investigate the potential linkage between high rate of p16 methylation and hepatitis B virus （HBV） infection, methylation status of p16, HBV infection markers in serum and HBV-DNA replication level in cancerous and non-cancerous tissue of 32 cases of hepatocellular carcinomas （HCC） with HBV infection and 12 HCCs without HBV infection were examined. Methods： p16 methylation was detected with methylation-specific polymerase Chain reaction （PCR）, and HBV markers were examined with real-time PCR and immunologic method. Results： Methylation of p16 promoter was found in 31 （70.5%） of 44 cancerous tissues of HCC, 2 （16.7%） of 12 HCC without HBV infection, 29 （90.6%） of 32 HCCs with HBV infection marker, p16 methylation was detected in 5 （83.3%） of 6 HCCs positive for HBsAg and HBeAg, 17 （94.4%） of 18 HCCs positive for HBsAg and negative for HBeAg, 7/8 （87.5%） of HCCs positive for other HBV infection markers, such as HBsAB, HBcAb, HBeAb. p16 methylation products were also found in non-cancerous tissues of 4 cases of HCCs with HBV infection, not detected in non-cancerous tissues without HBV infection. HBV-DNA was detected in cancerous tissues of 29/32 （90%） HCCs with HBV infection. Surprisingly, Methylation product of p16 promoter was found in all cases （29/29） of HCCs with detectable HBV-DNA in neoplastic tissue. Conclusion： Persistent HBV infection may promote p16 hypermethylation, suggesting that HBV, via enhancing the aberrant methylation of p16, indirectly involved in development of HCC.

A Preliminary Investigation on Anti-inflammatory and Antibacterial Effect of Compound Sarcandra Aerosol

[Objective] This study aimed to reveal the therapeutic mechanism of compound sarcandra aerosol, which was exclusively owned by the Second Affiliated Hospital of Guiyang College of Traditional Chinese Medicine. [Method] An inflammation model was established by xylene-induced inflammation test and carrageenan- induced inflammation test to analyze the anti-inflammatory effect of compound sarcandra aerosol. By bacteriostasis test in vitro, the antibacterial effect of compound sarcandra aerosol against five common pathogens of pharyngitis was investigated. Blood samples were collected from Wistar rats in different compound sarcandra aerosol groups and control group to compare blood routine indicators and interleukin-1 （IL-1） levels. [Result] Three different concentrations of compound sarcandra aerosol could reduce degrees of xylene-induced ear edema in mice and carrageenan- induced paw edema in rats, but the anti-inflammatory effect of compound sarcandra aerosol was reduced as the concentration declined. In bacteriostasis test in vitro, the minimum inhibitory concentration of compound sarcandra aerosol against Streptococcus pneumoniae, Streptococcus hemolytis, Corynebacterium diphtheriae, Staphylococcus aureus and Salmonella typhimurium was 76, 105 38, 65 and 30 mg/ml, respectively. Compound sarcandra aerosol reduced white blood cell count, neutrophil count and lymphocyte percentage in pharyngitis model rats. Moreover, interleukin-1 level in watermelon frost lozenge group and different compound sarcandra aerosol groups was lower compared with control group. [Conclusion] Compound sarcandra aerosol can effectively treat pharyngitis by exerting anti-inflammatory and antibacterial effect and reducing interleukin-1 level. This study laid a solid foundation for clinical application of compound sarcandra aerosol.

Ultrastructural observation on the relation of H.pylori to the gastric epithelia in chronic gastrictis and in peptic ulcer

AIMS The relationship between Helicobacter pylori (Hp) and gastric epithelia in chronic gastritis and in petic ulcer was studied by transmission electron mi- croscopy (TEM). METHODS Seventy-five gastric antral biopsy speci- mens from the patients examined by six other methods for Hp were fixed in glutaraldehyde and treated with tanin acid before OsO_4 staining than routinely prooessed for TEM studies (at least 4 semi- thin sections oriented for ultrathin sections in each sample). RESULTS The bacilli were detected by TEM within gastric mucosa in 53 of 55 patients infected with Hp. Ultrathin sections especially stained with tanin acid re- vealed clearly glycocalyx by which the bacillus was connected with the epithelium. As the bacilli grouped as colony and breed,the adjacent mucous cells degerated and characterized by erosion of the juxtalu- minal cytoplasm,vacuolation or blebs,even desqua- mation of cell. Evidence was accumulated to show that the baoilli were located in the lumen attracted neu- trophils which intended to migrate into intercellular space of epithelia or into the lumen to exert the effect of Hp phagocytosis. CONCLUSIONS The sensitivity and specificity of Hp diagnosis by TEM is respectively 96% and 95%. Tanin acid is suitable for the preservation of glycocalyx of cell. The colonized bacilli,usually with the wide periplasmic pools,contributed to the spectrum degen- eration of epithelia,including mucous neck cells. If Hp infection persists,the degeneration and regeneration of mucous neck cells alternatively carried on and ultimate- ly the generative stem cells were damaged,as the result,the chronic atrophy gastritis could occure.

Pathogenesis of Parkinson＇s disease： oxidative stress, environmental impact factors and inflammatory processes

Current hypothesis of neuronal degeneration in Parkinson＇s disease （PD） have been proposed, including formation of free radicals and oxidative stress, mitochondrial dysfunction, excitotoxicity, trophic factor deficiency, inflammatory processes, genetic factors, environmental impact factors, toxic action of nitric oxide, apoptosis, and so on. This review mainly discussed oxidative stress, environmental impact factors, and inflammatory processes in PD.

Cellular immune function and liver damage in post hepatitic cirrhosis

AIM To study the cellular immune function in patients with post hepatitic cirrhosis (PHC) and its relation with different liver damages.

Lipopolysaccharide-induced cerebral inflammatory damage and the therapeutic effect of platelet activating factor receptor antoganist

Objective To investigate lipopolysaccharide （LPS） induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B （BN52021）. Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups （n = 10 for each group）： Control group, Model group and Treatment group （treated with BN52021）. LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method. Results The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly. Conclusion LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.

基于三焦辨证探讨腹泻型肠易激综合征(中焦脾虚湿热证)的中医发病机制及治疗

肠易激综合征(irritable bowel syndrome,IBS)是一种较为多见的慢性胃肠道功能紊乱性疾病,其中腹泻型最为常见。目前临床上尚无确切疗效的药物,加之其病情迁延难愈,时刻困扰着患者及医务工作者。然而中医在肠易激综合征的治疗方面有着良好的疗效。文章基于三焦辨证阐述腹泻型肠易激综合征的病因病机认识,以及介绍杨勤主任中医师为治疗腹泻型肠易激综合征所创制的清化肠炎方组成、配伍意义、临床应用等,以期为临床肠易激综合征的中医诊疗提供新思路。

Role of cytokines in inflammatory bowel disease

Inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), rep- resents a group of chronic disorders characterized by inflammation of the gastrointestinal tract, typically with a relapsing and remitting clinical course. Mucosal mac- rophages play an important role in the mucosal im- mune system, and an increase in the number of newly recruited monocytes and activated macrophages has been noted in the inflamed gut of patients with IBD. Activated macrophages are thought to be major con- tributors to the production of inflammatory cytokines in the gut, and imbalance of cytokines is contributing to the pathogenesis of IBD. The intestinal inflammation in IBD is controlled by a complex interplay of innate and adaptive immune mechanisms. Cytokines play a key role in IBD that determine T cell differentiation of Th1, Th2, T regulatory and newly described Th17 cells. Cytokines levels in time and space orchestrate the development, recurrence and exacerbation of the inflammatory process in IBD. Therefore, several cyto- kine therapies have been developed and tested for the treatment of IBD patients.

Different cell kinetic changes in rat stomach cancer after treatment with celecoxib or indomethacin: Implications on chemoprevention

AIM: Mechanisms underlying the chemopreventive effects of cyclooxygenase (COX) inhibitors remain elusive. We have previously shown that celecoxib but not indomethacin could prevent carcinogen-induced gastric cancer development in Wistar rats. This chemopreventive effect appeared to be independent of COX-2 and prostaglandin (PG) E2 suppression since the lowest PGE2 was obtained in indomethacin group.This study compared the cell kinetic changes in stomachs of rats after treatment with celecoxib (5, 10, 20 mg/(kg·d)) or indomethacin (3 mg/(kg·d)) to gain more insights into the chemopreventive mechanism.METHODS: The apoptosis and proliferation indexes in gastric tumor, adjacent non-cancer tissues and normal gastric tissues were determined. Apoptosis was quantified by apoptotic nuclei counting and TUNEL, whereas proliferation was determined by Ki67 immunostaining.RESULTS: Treatment with either celecoxib or indomethacin inhibited gastric tumor proliferation by more than 65% (P＜0.02). However, celecoxib caused a dose-dependent increase in apoptosis (P＜0.05) which was not seen in indomethacin-treated tumors (P = 0.54). The highest apoptosis to proliferation ratio was seen in tumors treated with celecoxib at 10 mg/(kg·d). Treatment with this dose of celecoxib was associated with the lowest incidence of gastric cancer development.CONCLUSION: Our findings suggest that the difference in chemopreventive effects of indomethacin and celecoxib in this animal model of gastric carcinogenesis is largely due to the differential cell kinetic changes, which does not correlate with the degree of COX-2 and PG suppression.

Dietary and metabolomic determinants of relapse in ulcerative colitis patients: A pilot prospective cohort study

AIM To identify demographic, clinical, metabolomic, and lifestyle related predictors of relapse in adult ulcerative colitis(UC) patients.METHODS In this prospective pilot study, UC patients in clinical remission were recruited and followed-up at 12 mo to assess a clinical relapse, or not. At baseline information on demographic and clinical parameters was collected. Serum and urine samples were collected for analysis of metabolomic assays using a combined direct infusion/liquid chromatography tandem mass spectrometry and nuclear magnetic resolution spectroscopy. Stool samples were also collected to measure fecal calprotectin(FCP). Dietary assessment was performed using a validated self-administered food frequency questionnaire. RESULTS Twenty patients were included(mean age: 42.7 ± 14.8 years, females: 55%). Seven patients(35%) experienced a clinical relapse during the follow-up period. While 6 patients(66.7%) with normal body weight developed a clinical relapse, 1 UC patient(9.1%) who was overweight/obese relapsed during the follow-up(P = 0.02). At baseline, poultry intake was significantly higher in patients who were still in remission during follow-up(0.9 oz vs 0.2 oz, P = 0.002). Five patients(71.4%) with FCP > 150 μg/g and 2 patients(15.4%) with normal FCP(≤ 150 μg/g) at baseline relapsed during the follow-up(P = 0.02). Interestingly, baseline urinary and serum metabolomic profiling of UC patients with or without clinical relapse within 12 mo showed a significant difference. The most important metabolites that were responsible for this discrimination were trans-aconitate, cystine and acetamide in urine, and 3-hydroxybutyrate, acetoacetate and acetone in serum. CONCLUSION A combination of baseline dietary intake, fecal calprotectin, and metabolomic factors are associated with risk of UC clinical relapse within 12 mo.

Clinical features and management of primary sclerosing cholangitis

Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by inflammation and fibrosis of the bile ducts,resulting in cirrhosis and need for liver transplantation and reduced life expectancy.The majority of cases occur in young and middle-aged men,often in association with inflammatory bowel disease.The etiology of primary sclerosing cholangitis includes immune-mediated components and elements of undefined nature.No effective medical therapy has been identified.The multiple complications of primary sclerosing cholangitis include metabolic bone disease,dominant strictures,bacterial cholangitis,and malignancy,particularly cholangiocarcinoma,which is the most lethal complication of primary sclerosing cholangitis.Liver transplantation is currently the only life-extending therapeutic alternative for patients with end-stage disease,although recurrence in the allografted liver has been described.A PSC-like variant attracting attention is cholangitis marked by raised levels of the immunoglobulin G4 subclass,prominence of plasma cells within the lesions,and steroid responsiveness.

Ameliorative effects of bombesin and neurotensin on trinitrobenzene sulphonic acid-induced colitis,oxidative damage and apoptosis in rats

AIM:To investigate the effects of bombesin (BBS) and neurotensin (NTS) on apoptosis and colitis in an ulcerative colitis model. METHODS:In this study, a total of 50 rats were divided equally into 5 groups. In the control group, no colitis induction or drug administration was performed. Colitis was induced in all other groups. Following the induction of colitis, BBS, NTS or both were applied to three groups of rats. The remaining group (colitis group) received no treatment. On the 11th d after induction of colitis and drug treatment, blood samples were collected for TNF-α and IL-6 level studies. Malondialdehyde (MDA), carbonyl, myeloperoxidase (MPO) and caspase-3 activities, as well as histopathological findings, evaluated in colonic tissues. RESULTS:According to the macroscopic and microscopic findings, the study groups treated with BBS, NTS and BBS + NTS showed significantly lower damage and inflammation compared with the colitis group (macroscopic score, 2.1 ± 0.87, 3.7 ± 0.94 and 2.1 ± 0.87 vs 7.3 ± 0.94;microscopic score, 2.0 ± 0.66, 3.3 ± 0.82 and 1.8 ± 0.63 vs 5.2 ± 0.78, P < 0.01). TNF-α and IL-6 levels were increased significantly in all groups compared with the control group. These increases were significantly smaller in the BBS, NTS and BBS + NTS groups compared with the colitis group (TNF-α levels, 169.69 ± 53.56, 245.86 ± 64.85 and 175.54 ± 42.19 vs 556.44 ± 49.82;IL-6 levels, 443.30 ± 53.99, 612.80 ± 70.39 and 396.80 ± 78.43 vs 1505.90 ± 222.23, P < 0.05). The colonic MPO and MDA levels were significantly lower in control, BBS, NTS and BBS + NTS groups than in the colitis group (MPO levels, 24.36 ± 8.10, 40.51 ± 8.67 and 25.83 ± 6.43 vs 161.47 ± 38.24;MDA levels, 4.70 ± 1.41, 6.55 ± 1.12 and 4.51 ± 0.54 vs 15.60 ± 1.88, P < 0.05). Carbonyl content and caspase-3 levels were higher in the colitis and NTS groups than in control, BBS and BBS + NTS groups (carbonyl levels, 553.99 ± 59.58 and 336.26 ± 35.72 vs 209.76 ± 30.92, 219.76 ± 25.77 and 220.34 ± 36.95;caspase-3 levels, 451.70 ± 68.27 and 216.20 ± 28.17 vs 28.60 ± 6.46, 170.50 ± 32.37 and 166.50 ± 30.95, P < 0.05). CONCLUSION:The results of this study suggest BBS and NTS, through their anti-inflammatory actions, support the maintenance of colonic integrity and merit consideration as potential agents for ameliorating colonic inflammation.

Seasonal variation in the onset of acute pancreatitis

AIM:A drcannual variation in the onset of several acute diseases, mostly dealing with cardiovascular system,has been reported. The present study was to verify the possible existence of a seasonal variability in the onset of acute pancreatitis. METHODS:All patients consecutively admitted to the Hospital of Ferrara,Italy,between January 1998 to December 2002, whose discharge diagnosis was acute pancreatitis,were considered.According to the time of admission,cases were categorized into twelve 1-mo intervals and in four periods by season.x^2 test for goodness of fit and partial Fourier series were used for statistical analysis. RESULTS:During the study period,549 cases of acute pancreatitis were observed.A significant peak of higher incidence was found in March-May,both for total population, males and subgroups with and without cholelithiasis or alcoholism.Fourier analysis showed the existence of a circannual rhythmic pattern with its main peak in March(95% CL.:February-April,P=0.005),and a secondary one in September.Death occurred more frequently in December- February,compared to the other periods(P=0.029),and chronobiologic analysis yielded a seasonal peak in November- December(P<0.001). CONCLUSION:This study shows the existence of a circannual variation in the onset of acute pancreatitis,with a significantly higher frequency of events in the spring,especially for patients with cholelithiasis or alcoholism.Moreover,events occurring during the colder months seem to be characterized by a higher mortality rate.

L-arginine-induced experimental pancreatitis

Despite medical treatment,the lethality of severe acute pancreatitis is still high (20-30%).Therefore,it is very important to find good animal models to characterise the events of this severe disease.In 1984,Mizunuma et al. developed a new type of experimental necrotizing pancreatitis by intraperitoneal administration of a high dose of L-arginine in rats.This non-invasive model is highly reproducible and produces selective,dose-dependent acinar cell necrosis. Not only is this a good model to study the pathomechanisms of acute necrotizing pancreatitis,but it is also excellent to observe and influence the time course changes of the disease.By writing this review we iluminate some new aspects of cell physiology and pathology of acute necrotizing pancreatitis.Unfortunately,the reviews about acute experimental pancreatitis usually did not discuss this model. Therefore,the aim of this manuscript was to summarise the observations and address some challenges for the future in L-arginine-induced pancreatitis.

Pathogenesis of Parkinson’s disease: oxidative stress, environmental impact factors and inflammatory processes

Current hypothesis of neuronal degeneration in Parkinson’s disease (PD) have been proposed, including formation of free radicals and oxidative stress, mitochondrial dysfunction, excitotoxicity, trophic factor deficiency, inflam- matory processes, genetic factors, environmental impact factors, toxic action of nitric oxide, apoptosis, and so on. This review mainly discussed oxidative stress, environmental impact factors, and inflammatory processes in PD.

Effects of octreotide on acute necrotizing pancreatitis in rabbits

AIM:To assess the role of oxygen-derived free radicals and cytokines in the pathogenesis of taurocholic acid-induced acute pancreatitis,and to evaluate the preventive effects of octreotide towards the development of acute pancreatitis. METHODS:Acute pancreatitis was induced in male New Zealand white rabbits by retrograde injection of 0.8 mL/kg·b.m,of 50 g/L sodium taurocholate (NaTC) in the pancreatic duct.Sham- operated animals served as control.Octreotide i mg/kg·b.m. was administered subcutaneously before the induction of pancreatitis.Blood was taken from the jugular vein before and at 1,3,6,12 and 24 h after pancreatitis induction. Serum activities of amylase,IL-6 and TNF-α and levels of malonyl dialdehyde (MDA),glutathione (GSH),glutathione peroxidase (GPx),catalase and superoxide dismutase (Mn-, Cu-,and Zn-SOD) in pancreatic tissue were measured. RESULTS:Serum TNF-α and IL-6 levels increased significantly 3 h after the onset of pancreatitis,and then returned to control level.The tissue concentration of MDA was significantly elevated at 24 h,while the GSH level and GP-x,catalase,Mn-SOD,Cu-,Zn-SOD activities were all significantly decreased in animals with pancreatitis as compared to the control.Octreotide pretreatmnent significantly reversed the changes in cytokines and reactive oxygen metabolites.Octreotide treatment did not alter the serum amylase activity and did not have any beneficial effects on the development of histopathological changes. CONCLUSION:Oxygen-derived free radicals and proinflammatory cytokines are generated at an early stage of NaTc-induced acute pancreatitis in rabbits.Prophylactic octreotide treatment can prevent release of cytokines and generation of reactive oxygen metabolites,but does not have any beneficial effects on the development of necrotizing pancreatitis.