The etiology and pathogenesis of inflammatory bowel disease are up to now still not clear and definite. Establishing the ideal animal model to study its cause and pathogenesis of this disease is very important. The ideal animal model should have the same manifestation with human inflammatory bowel disease on clinical and pathologic feature etc. In this article, the method, the pathologic character istics and concerning pathogenesis, of a few common useful experiment animal models are discussed. [

Objective To investigate lipopolysaccharide (LPS) stimulates the expression of nuclear factor-KB (NF-κB) mRNA and tumor necrosis factor-a( TNF-α) mRNA in rat's pancreatic acinus AR42J cell line, and further address the pathogenesis of acute pancreatitis. Method The AR42J cell line was stimulated with different concentrations of LPS (0.001, 0.01, 0.1, 1.0, 10 and 100 mg/L) for 18 hours, or stimulated with 10 mg/L of LPS for different lengths of time (2, 6, 12,18 and 24 hrs) .Then, the expressions of NF-κB-P65 mRNA and TNF-α mRNA were determined by using RT-PCR, the levels of TNF-α protein in the culture supernatant were measured with radio-immuno assay (RIA), and the correlation between the expressions of TNF-α mRNA and NF-κB mRNA was analyzed. Results Both the expressions of NF-κB mRNA and TNF-α mRNA were up-regulated when AR42J cell line was stimulated with 10 mg/L of LPS for 2 hours or with 0.001 mg/L of LPS for 18 hours in both dose-dependent and time-dependent manners. Similarly, the levels of TNF-α protein were up-regulated when AR42J cell line was stimulated with 0.01 mg/L of LPS for 18 hours or with 10 mg/L of LPS for 6 hours in both dose-dependent and time-dependent manners. Statistical analysis revealed the positive correlation between the expressions of TNF-α mRNA and NF-κB-P65 mRNA(r = 0.962, P < 0.01). Conclusions LPS stimulates the expressions of TNF-α mRNA and NF-κB mRNA in both dose-dependent and time-dependent manners, and their expressions are closely correlated, suggesting the inhibition of their expressions as a potential therapeutic target for acute panceatitis.

OBJECTIVETo explore the effect of Qingyi Granule (QYG) on high mobility group box-1 (HMGB1) expressions in liver and renal tissues of severe acute pancreatitis (SAP) rats.

METHODSFifty-four Sprague-Dawley (SD) rats were divided into the sham-operation (SO) group, the SAP group, and the QYG group according to random digits table. Rats in the SAP group were induced by injecting 5% sodium taurocholate (STC). Liver and renal pathological changes were observed by HE staining. Serum contents of amylase (AMS), MDA, IL-1, and HMGB1 were detected by ELISA. HMGB1 protein expressions in liver and renal tissues were tested by immunohistochemistry. HMGB1 mRNA expressions in liver and renal tissues were detected by reversed transcription PCR.

RESULTSThe pathological scores, serum levels of AMS, MDA, IL-1 and HMGB1, and protein and mRNA HMGB1 expressions in liver and renal tissues were increased more obviously in the SAP group than in the SO group (P < 0.05, P < 0.01). All of them could be down-regulated by QYG intervention, with the most significant effect seen at 72 h (P < 0.05, P < 0.01) in a time-effect relationship.

CONCLUSIONSHMGB1 participated in SAP complicated liver and renal injuries. QYG could effectively inhibit HMGB1 expressions, thereby attenuating SAP complicated liver and renal injuries.

Amylases ; Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; HMGB1 Protein ; metabolism ; Interleukin-1 ; Kidney ; metabolism ; Liver ; metabolism ; Pancreatitis ; drug therapy ; metabolism ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Taurocholic Acid

Objective To study what affect the incidence and recurrence of keloids. Methods A total of 476 cases were treated with surgery plus adjunctive radiation therapy, intraleisional injection of triamcinolone acetonaide acetate, or surgery plus postoperative topical medicine. The family history and other clinical data were analyzed, including patients' age, sex, the duration of keloids, initiating factors, location, size, treatment method, and recurrence of the keloids. Results Keloids occurred in both male and female with the rate of 1. 83 ∶ 1. 00, with a predominance in woman aged from 22 to 45 years old. Trauma and pierce were the most significant initiating factors. The recurrence was affected by patients family history, treatment methods and the location of keloids, and less affected by keloids size, patients' age and sex. Conclusions Both surgery following adjunctive radiation therapy and intraleisional Kenalog injection are useful methods, which are prior to surgery plus postoperative topical medicine. The keloids incidence has a preponderance in some patients with family history. Therefore,genetic research is important to identify the pathogenetic factors in the keloids.

AIM: To investigate DNA-binding activity of nuclear factor ka ppa B (NF-?B) and pyrrolidine dithiocarbamate (PDTC) anti-inflammation effect and mechanism in trinitrobenzene sulfonic acid (TNBS)-induced acute colitis in rats. METHODS: Acute colitis was induced by instilling TNBS/ ethanol into the lumen of the rat colon. Rats were randomized into PDTC-treat g roup (including group P10,P25,P50,P100), TNBS/ethanol group and normal control g roup. The rats in PDTC-treated group were injected intraperitoneally with PDTC at the dosages of 10, 25, 50, and 100 mg?kg -1 , respectively. Rats wer e killed at 4 h after enema. Colonic inflammation, the ratio of wet/dry weig ht and MPO, SOD, and MDA activity were detected. DNA-binding activity of NF-? B was assessed by EMSA. RESULTS: NF-?B activity in colon homog enate was increased markedly at acute colitis in rats. PDTC attenuates the devel opment of rat colonic inflammation but not by reducing the NF-?B activity. CONCLUSION: NF-?B is activated in rats with acute colitis, which may be a mechanism of self-protection. PDTC can attenuate the development of in flammation.

AIM To establish a new, simple, stable and classical experimental model of acute edematous pancreatitis. METHODS Male mice were injected intraperitoneally 2?200 mg?(100 g) -1 body weight of L-arginine in an 1 h interval, as a 20% solution in 0.15 mol?L -1 NaCl. Control mice received the same quantity of 0.15 mol?L -1 NaCl. The mice were killed at 6, 12, 24, 48, 72 h following L-arginine administration. The serum amylase level, wet/dry weight ratio of the pancreas, histologic were assessed. RESULTS The serum level of amylase was significantly elevated at 6 h,reached the peak level at 24 h, normalized at 72 h. Histologic examination revealed interstitial edema and inflammatory cell infiltration reached the peak level at 24 h and decreased at 48,72 h. The wet/dry weight ratio of the pancreas changed in accordance with the interstitial edema. CONCLUSIONS The present study has demonstrated that the administration of excessive doses of arginine induces a new, noninvasive experimental model of acute edematous pancreatitis.

Objective To investigate the effects of Tat-NBD(NEMO-binding domain,NBD)peptide on LPS-stimulated AR42J acinus cells inflammatory response.Method Lipopolysaccharide(LPS)was added to culture media at doses of 10 mg/kg for 24 hours to stimulate the AR42J cells.For pretreatment.cells were incubated with different peptides for 2 hours before LPS stimulation.The expression of TNF-α mRNA WaS conducted using a semi-quantitative RT-PCR method.TNF-α protein in culture medium were detected by enzyme linked immunosorbent assay(ELISA).The expression and translocation of the NF-kB-p65 protein of AR42J was determined by Strept Actividin-Biotin Complex(SABC)method.Results LPS(10 mg/L)resulted in an increase of TNF-αmRNA and TNF-αprotein,whereas significant inhibitory effects were observed when cells were incubated with Tat-NBD(WT)just on dose of 0.1 me/L(P＜0.05).The Tat-NBD(WT)peptide decreased inflammatory cytokine expression by a dose-dependent manner and its peak role was on dose of 100 mg/L.Consisting with TNF-α expression decrease,NF-kB-p65 expression signitieantly decreased in Tat-NBD(WT)pretreatment group,especially on the largest dose.NO significant changes in the control peptide group.Conclusions Tat-NBD(WT)peptide can inhibit the inflammation of acinus simulated by LPS.

Aim To research the influence of the animals pruritus model by used pruritus medium with histamine,dextran 40 or 4-aminopyridine(4-AP),and to establish a new pruritus model.Methods The orthogonal test was used to array the experiment.In the experiment different pruritus mediums were hypodermically injected for 0.1 ml in the depilated area,the scratching incubation period and scratching number in 30 minutes were counted after the injection.The best pruritus group was screened out by synthesis grading law.The injected skin area in each group was located out to be determined the histamine contents in it.Results The best model group was the combination of histamine and 4-aminopyridine.Compared with the blank group,the scratching number and scratching incubation period of other pruritus model groups in 30 minutes were of significant difference(P

Objective To investigate the distribution of hepatitis B virus(HBV)genotypes in Zhejiang.Methods HBV genotyps were detected by fluorimetric real-time PCR in 240 HBVDNA positive patients who were born in Zhejiang(Hangzhou,Huzhou,Jinhua,Shaoxing,Taizhou,Ningbo each 40 positive patients).Results of the 240 HNBDNA positive patients,82(34.17%)were genotype B,and 140(58.33%)were genotype C,15(6.25%)were genotype B and C,3(1.25%)were genotype D.No genotype A、E and F found in the studied subjects.Conclusions HBV genotype B,genotype C,genotype B and C,genotype D existed in Zhejiang and there is no difference in ferms of the distribution of genotypes in six areas metioned above.

Objective To clarify the role of transmembrane protein 66(TMEM66) in intima proliferation of carotid artery induced by balloon injury in rats.Methods SD rats were randomly divided into three groups (n=10), including control group, the left carotid artery balloon injury group and injury group added with lentiviruses, respectively.Accordingly, the intima proliferation of carotid artery were detected by H/E staining;the expressions of TMEM66 in carotid artery injuried by balloon were determined by Western blot,q-PCR and immunohistochemistry, and the migration and proliferation of VSMCs were measured by scratch test and CCK8 respectively.Results Compared with control group, the expression of TMEM66 in carotid artery was obviously decreased after balloon injury (P<0.05).Most importantly, the intima proliferation of carotid artery was significantly reversed by overexpression of TMEM66 via specific lentiviruses (P<0.05).Conclusions TMEM66 is able to attenuate the intima proliferation of carotid artery after balloon injury.It could be that upregulation of TMEM66 can alleviate the migration and proliferation of VSMCs by PDGF.