ObjectiveTo investigate the effect of nitric oxide(NO) in preventing postoperative adhesion formation in rats .MethodsForty rats were randomly assigned to 2 different treatment groups.All animal models of postoperative adhesion formation were made in a standard manner. 0.9% NaCl and L-arginine were administered into intraperitoneal cavity before closure and during 3 consecutive days after surgery. On the 3 rd postoperative day,blood was collected to evaluate NO levels and the inserted abdominal walls were removed to assess pathology in some rats.On the 14 th postoperative day,the remaining rats were sacrificed by ether overdose before relaparotomy,and the extent of adhesion formation were assessed.ResultsMore severe adhesions developed in 0.9% NaCl control group(mean score of adhesions 3.7?0.7) than L-arginine group(mean score of adhesions 0.9?1.1)( P

Objective To study the effects of peroxisome proliferators-activated receptor gamma (PPA?r) on the biological characteristics of hepatic stellate cells (HSCs); Methods The activated HSCs were divided into four groups: control group, rosiglitazone group, GW9662 + rosiglitazone group and GW9662 group. The cell proliferation was determined with MTT colorimetric assay, The cell apoptosis was studied with flow cytometry. The expression of PPA?r, Type I collagen were detected by RT-PCR, Western blot and immunocytochemistry. Results MTT of HSCs in rosiglitazone group was (0. 49?0. 06) significantly lower than in control group ( 1. 00?0. 045 ), GW9662 group (0. 89?0. 043 ) , GW9662 + rosiglitazone group (0.78?0.049)(t = 15.59,14.68,8.07, P

Objective To study the effect of rosiglitazone, a ligand of peroxisome proliferator-activated receptor gamma (PPAR?), on the expression of PPAR? in hepatic stellate cells (HSCs) and its effect on the biological characters of HSCs. Methods The activated HSCs were devided into three groups:control, 3??mol/L rosiglitazone group, and 10??mol/L rosiglitazone group. The expression of PPAR?, ?-smooth muscle actin(?-SMA), and type Ⅰ and Ⅲ collagen was detected by means of RT-PCR, Western blot and immunocytochemistry respectively. The cell proliferation was determined with MTT colorimetric assay. The cell apoptosis was demonstrated with flow cytometry. Results The expression of PPAR? at mRNA and protein level markedly increased in HSCs of 10??mol/L rosiglitazone group(t≥4.627, P

Objective To study the effect of peroxisome proliferator-activated receptor garama (PPARγ) ligand on hepatic fibrosis in rats. Methods Forty Wistar rats were randomly divided into two groups: the control group(20 rats) ,in which liver cirrhosis was induced by adding 0. 3‰ thioacetamide in the fodder for 6 months, and rosiglitazone group(20 rats) in which 200 ppm of rosiglitazone in combination with 0. 3‰ thioacetamide was added in the fodder. Liver tissue's mRNA expression of PPARγ, TGF-β1 ,type Ⅰ pro-collagen and α-smooth muscle actin(α-SMA) was detected by RT-PCR. The protein expression of PPARγ, TGF-β1 ,type Ⅰ collagen and α-SMA was detected by Western blot. The expression of collagenof liver histological section was evaluated by Van Gieson (VG) staining. Results The expression ofPPARγ at mRNA level significantly increased in rosiglitazone group compared with those in the control group ( t = 6. 93, P < 0. 01 ), while the expression of TGF-β1 ( t = 3. 89, P < 0. 01 ) and type Ⅰ pro-collagen ( t =5.67,P <0. 01 ) were lower than that in the control group. The protein expression of PPARγ, TGF-β1 and type Ⅰ collagen was in similar tendence with that of mRNA expression. The expression of α-SMA decreased significantly in rosiglitazone group compared with that in the control group (t = 3. 12,P < 0.01 ). The collagen stainings of liver histological section in rosiglitazone group was lower than those in the control group (t = 3.47, P < 0. 01 ). Conclusion PPARγ ligand inhibits the production of collagen in fibrofic livers in rats and prevents hepatic fibrosis in vivo.

Objective To investigate the mRNA and protein expression of somatostatin receptors in hepatocellular carcinoma HCCLM3 cell lines and to explore the mechanism by which somatostatin effects on hepatocellular carcinoma. Methods RT-PCR., immunocytochemistry and MTT were used to detect mRNA and protein expression of somatostatin receptors in hepatocellular carcinoma cells and evaluate the antiproliferative effect of somatostatin. Results The effect of somatostatin on the cellular proliferation was verified. Immunocytochemistry study revealed a mainly intracellular distribution of all SSTRs with unique patterns for each of them. mRNA expression of all 5 subtypes of somatostatin receptors was different, SSTR2 and SSTR1 mRNA expressions were significantly higher than SSTR3, SSTR4 and SSTR5 ( P