OBJECTIVETo evaluate the effect of sodium tanshinone IIA sulfonate (STS) in preventing postoperative peritoneal adhesions in rats and explore the mechanisms.

METHODSSixty SD rats were randomized into 4 equal groups, including a blank control group, adhesion model group, and high-, moderate-, and low-dose STS-treated groups, and were subjected to injuries of the parietal peritoneum and cecum to induce peritoneal adhesions, followed by intraperitoneal administration of saline and STS at the doses of 20, 10, and 5 mg/kg for 7 consecutive days, respectively. Another 15 untreated rats served as the blank control group. The adhesion scores in each group were recorded after the treatments; the activity of tissue-type plasminogen activator (tPA) in peritoneal lavage fluid was measured, tPA/PAI-1 protein ratio in the peritoneal tissue was determined by ELISA, and the expressions of TGF-β1 and collagen I were detected by immunohistochemistry. The anastomotic healing model was used to assess the impact of STS on wound healing.

RESULTSIntraperitoneal administration of STS effectively prevented peritoneal adhesion without affecting anastomotic healing in the rats. Compared with the adhesion model group, the STS-treated groups showed increased peritoneal lavage fluid tPA activity and tPA/PAI-1 ratio in the ischemic tissues with lowered TGF-β1 and collagen I expressions in the ischemic tissues.

CONCLUSIONSIntraperitoneal administration of STS can prevent peritoneal adhesion and enhance local fibrinolysis in rats, and these effects may be mediated by TGF-β signaling pathway.

Animals ; Cecum ; injuries ; pathology ; Collagen Type I ; metabolism ; Fibrinolysis ; Injections, Intraperitoneal ; Peritoneum ; injuries ; pathology ; Phenanthrenes ; pharmacology ; Plasminogen Activator Inhibitor 1 ; metabolism ; Postoperative Complications ; prevention & control ; Rats ; Rats, Sprague-Dawley ; Tissue Adhesions ; prevention & control ; Tissue Plasminogen Activator ; metabolism ; Transforming Growth Factor beta1 ; metabolism ; Wound Healing

OBJECTIVETo observe the effect of Shenshuning Recipe (SR) on the peritoneal function, accumulation of extracellular matrix (ECM), and the expression of transforming growth factor-beta1 (TGF-beta1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the peritoneal fibrosis rats.

METHODSThe peritoneal fibrosis correlating peritoneal dialysis SD rat model was induced by injecting erythromycin and peritoneal dialysate. They were randomly divided into 4 groups according to body weight, i.e., the 1.50% peritoneal dialysate group (Group B), the 1.50% peritoneal dialysate + SR group (Group C), the 4.25% peritoneal dialysate group (Group D), and the 4.25% peritoneal dialysate +SR group (Group E), 15 in each group. Besides, another 15 rats was taken as the blank control group (n = 15, Group A). SR at the daily dose of 43.93 g/kg was given to rats in Group C and E by gastrogavage, while equal volume of normal saline was given to rats in other groups by gastrogavage. The changes of glucose in the peritoneal fluid were detected. The ultra filtration volume (UF)and mass transfer of glucose (MTG) were calculated. The pathomorphological changes of the peritoneum were observed. The distribution of collagen fiber, fibroblast count, collagen I (Col I), expressions of TIMP-1 and TGF-beta1 were determined.

RESULTSAt the end of the 6th week, statistical difference was shown in UF [(-3.3 +/- 14.2) mL] and [(-2.0 +/- 10.7) mL], MTG [(18.1 +/- 0.8) mmol/kg] and [(16.1 +/- 1.2) mmol/kg], collagen fiber [(4 721.3 +/- 541.0)%] and [(6502.7 +/- 877.4)%], fibroblast [(0.087 +/- 0.010)/mm2] and [(0.131 +/- 0.042)/mm2], Col I [(187.5 +/- 36.9)%] and [(289.7 +/- 95.6)%], TIMP-1 [(2.57 +/- 0.94)%] and [(3.63 +/- 0.29)%], and TGF-beta1 [(104.0 +/- 20.7) ng/L] and [(108.2 +/- 17.5) ng/L] between Group C and Group E, when compared with the peritoneal dialysate group at the same concentration (P < 0.05, P < 0.01).

CONCLUSIONSR could postpone the development of peritoneal fibrosis in peritoneal dialysis SD rats possibly through inhibiting expressions of TGF-beta1 and TIMP-1, and hindering the over-accumulation of ECM.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Extracellular Matrix ; drug effects ; Male ; Peritoneal Dialysis ; Peritoneal Fibrosis ; metabolism ; pathology ; Peritoneum ; drug effects ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVETo observe the features of lipid metabolism disorders of peritoneal dialysis(PD)patients and hemodialysis(HD)patients and explore the association of lipid metabolism disorder with peritoneum transport ability and mortality.

METHODSThe clinical data of 127 PD patients and 95 HD patients who had received regular dialysis for more than 3 months in Peking Union Medical College Hospital since March 2009 were retrospectively analyzed.Serum lipid profiles were tested.Serum hypersensitive C reactive protein(hsCRP)was examined by immune turbidimetric method.Serum carbohydrate antigen 125(CA125)and iPTH were detected by electrochemical luminescence method.Peritoneum transport ability was evaluated through peritoneal equilibration test(PET).After a 2-year follow-up,the levels of CA125 and the peritoneum transport abilities were compared between the baseline data and the end point,and the relationship between lipid disorder and the mortality was analyzed.

RESULTSAfter the 2-year follow-up,25(19.7%)PD patients died.The leading cause of death was congestive heart failure(56.0%),followed by myocardial infarction(12.0%),septic shock(12.0%),respiratory failure(8.0%),asphyxiation(8.0%),and gastrointestinal bleeding(4.0%).Compared with the survivors,the death patients were older(P=0.005),with significant lower albumin level(P=0.000)and pre-albumin level(P=0.001).However,there was no significant difference in other clinical features including body mass index(BMI),blood pressure,dialysis time,nPCR,iPTH,hemoglobin,hsCRP,and serum lipid level(all P>0.05).COX regression analysis showed that diabetes mellitus(P=0.030)and mean SBP(P=0.048)were significantly associated with the mortality of PD patients.At the baseline,the CA125 level in patients with high,high average,and low average transport status of peritoneum was(38.02±64.37),(21.21±19.41),and(17.55±23.2)U/ml,respectively(P=0.09).There was no association between the transport status and lipid(TC,TG and LDL).

CONCLUSIONSCongestive heart failure is the leading cause of death among PD patients.Diabetes and blood pressure are the dependent risk factors of mortality.Lipid disorder is associated with CA125,while its association with peritoneum transport ability or mortality was not found.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; C-Reactive Protein ; metabolism ; Cause of Death ; Female ; Hemodiafiltration ; mortality ; Humans ; Lipid Metabolism Disorders ; mortality ; Male ; Middle Aged ; Peritoneal Dialysis ; mortality ; Peritoneum ; metabolism ; physiopathology ; Risk Factors ; Young Adult

OBJECTIVETo study possible immunobiological potential of Osmunda japonica Thunb.

METHODSImmunomodulatory effects of ethanol extracts prepared from rhizomes of O. japonica and phenolic compounds isolated from the extracts were investigated under the in vitro conditions using the rat peritoneal cells (2×10(6)/mL; 24 h culture). Biosynthesis of nitric oxide (NO) was assayed by Griess reagent, production of prostaglandin E2 (PGE2) and secretion of cytokines were determined by enzyme-linked immunoabsorbent assay.

RESULTSThe extracts activated dose dependently, with the onset at 2.5-5 μmol/L concentrations, the high output NO production, and secretion of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Mild enhancement of NO was produced by the aldehyde-type phenolics 4-hydroxybenzaldehyde and 3,4-hydroxybenzaldehyde. In contrasts, the acetone-type phenolics 4-hydroxybenzalacetone and 3,4-hydroxybenzalacetone inhibited production of immune mediators including cytokines (TNF-α, IL-1β, IL-6), NO, and PGE2. The 3,4-hydroxybenzalacetone was more effective than 4-hydroxybenzaldehyde. The IC50s estimates ranged within the interval of 5-10 μmol/L. No signs of cytotoxicity were observed up to the 50 μmol/L concentration of the compounds.

CONCLUSIONPhenolic compounds contained in medicinal herb Osmunda japonica possess distinct immunomodulatory activity.

Animals ; Cell Survival ; drug effects ; Cells, Cultured ; Dinoprostone ; biosynthesis ; Female ; Ferns ; chemistry ; Immunologic Factors ; pharmacology ; Interferon-gamma ; pharmacology ; Lipopolysaccharides ; pharmacology ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase Type II ; genetics ; metabolism ; Peritoneum ; cytology ; drug effects ; Phenols ; chemistry ; isolation & purification ; pharmacology ; Plant Extracts ; chemistry ; isolation & purification ; pharmacology ; Polymyxin B ; pharmacology ; Proline ; analogs & derivatives ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Thiocarbamates ; pharmacology

No abstract available.
Antigens, CD/metabolism ; Cell Adhesion Molecules/metabolism ; Female ; Humans ; Immunohistochemistry ; Peritoneum/metabolism/pathology ; Sarcoma, Ewing/*diagnosis/pathology/radiography ; Tomography, X-Ray Computed ; Young Adult

OBJECTIVETo study the effects of advanced glycosylation end products (AGEs) on the production of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) in vitro and the role of protein kinase C (PKC) in this course.

METHODSThe AGE-human serum albumin (HSA) (0, 100, 500, 1 000 microg/ml) was used in culture medium to stimulate the HPMC. The mRNA level of FN was measured with real-time PCR, moreover, the protein level of FN in HPMC was detected by ELISA. With the method of ELISA, the PKC activities were observed. Inhibitors or activators of PKC were used to observe the roles of PKC pathways on the AGE-HSA stimulated productions of FN in HPMC.

RESULTSAGE-HSA activated PKC in HPMC in a dose, time-dependent manner (P < 0.05). AGE-HSA up-regulated the expression of FN mRAN and protein in dose- and time-dependently (P < 0.01); PKC activator phorbol 12-myristate 13-acetate (PMA) induced FN expression, respectively depletion of PKC and calphostin C, a PKC inhibitor, effectively prevented both PMA and AGE-HSA-induced expression of the FN (P < 0.05).

CONCLUSIONAGEs can increase the activities of PKC. AGEs can directly increase FN expression in HPMC which may contribute to peritoneal fibrosis and this is regulated by PKC.

Cells, Cultured ; Epithelium ; secretion ; Fibronectins ; metabolism ; Glycation End Products, Advanced ; pharmacology ; Humans ; Peritoneum ; cytology ; Protein Kinase C ; metabolism

OBJECTIVETo assess the influence of laparoscopic colorectal cancer resection on the peritoneal microstructure injury and expression of t-PA/PAI-1 molecules.

METHODSA total of 50 patients with colorectal cancer were prospectively enrolled between June 2011 and February 2012 in the Shanxi Provincial Hospital and were assigned into laparoscopic group (LO, n=27) and conventional laparotomy group (CO, n=23) based on patients expectancy and surgeon decision. Optical microscope and scanning electron microscope were employed for comparison of the postoperative peritoneal injury between LO and CO. Before and after surgery, t-PA and PAI-1 of peritoneal tissue were determined by ELISA in both groups.

RESULTSOptical microscope and scanning electronic microscopy scan indicated less serosal injury in LO group than that in CO group with regard to serosa integrity, continuity of covering adipocytes and mesothelial cells, and the aggregation level of inflammatory cells (P<0.01). The injury score was 38.22 in CO in and 14.67 in LO and the difference was statistically significant (P<0.01). No significant differences were found between LO and CO in terms of postoperative t-PA in the omentum, t-PA and PAI-1 in the intestinal serosa tissue (P>0.05), however PAI-1 in the omentum was significantly lower in LO group compared to CO group (P<0.05).

CONCLUSIONLaparoscopic radical resection for colorectal cancer causes less peritoneal structural injury and less influence on the fibrinolytic capacity, which may contribute to less postoperative adhesion.

Adolescent ; Adult ; Aged ; Colorectal Neoplasms ; metabolism ; surgery ; Colorectal Surgery ; adverse effects ; methods ; Female ; Humans ; Laparoscopy ; adverse effects ; Male ; Middle Aged ; Peritoneum ; metabolism ; pathology ; Plasminogen Activator Inhibitor 1 ; metabolism ; Prospective Studies ; Tissue Plasminogen Activator ; metabolism ; Young Adult

OBJECTIVE: To investigate the expression of galectin-1 with the stimulation of peritoneal dialysis solution (PDS) and its role in the epithelial-to-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs). METHODS: HPMCs were stimulated with PDS containing different concentrations of high glucose (1.5%, 2.5%, and 4.25%). After 24 h, mRNA and protein expressions of galectin-1,vimentin, and zo-1 were analyzed with real-time PCR and Western blot, respectively. Liposome transfected siRNA technique was used to knock down the expression of galectin-1 and the effect of galectin-1 siRNA on the EMT of HPMCs was also observed under 4.25% PDS condition. RESULTS: mRNA expression of galectin-1 in HPMCs increased in PDS groups, especially in group with 4.25% PDS (P<0.05). Protein expression of galectin-1 in HPMCs significantly increased in PDS groups with a dose dependent manner (P<0.05).Expression of vimentin in HPMCs significantly increased in PDS groups, especially in groups of 2.5% PDS and 4.25% PDS (P<0.05), but zo-1 expression markedly decreased (P<0.05). The expression of galectin-1 correlated positively with vimentin (P<0.05) but negatively with zo-1 (P<0.05). Expression of vimentin in groups of 4.25% PDS was markedly inhibited (P<0.05) by galectin-1 siRNA, whereas zo-1 expression was significantly increased (P<0.05). CONCLUSION Galectin-1 can mediate high glucose PDS-induced EMT in HPMCs and may be a new target for the prevention and treatment of peritoneal fibrosis.
Cells, Cultured ; Dialysis Solutions ; pharmacology ; Epithelial Cells ; cytology ; Epithelial-Mesenchymal Transition ; drug effects ; Galectin 1 ; genetics ; metabolism ; Glucose ; pharmacology ; Humans ; Peritoneal Dialysis ; adverse effects ; Peritoneal Fibrosis ; etiology ; Peritoneum ; cytology ; RNA, Messenger ; genetics ; metabolism

OBJECTIVE: To investigate the possible role of Danshensu on fibronectin (FN) and collagen-I (Col-I) secretion induced by high glucose in human peritoneal mesothelial cells (HPMCs). METHODS: HPMCs were treated with high glucose and Danshensu at different concentrations. The mRNA expression of FN, Col-I, endothelin-1 (ET-1), and heme oxygenase-1 (HO-1) were examined by reverse transcription-polymerase chain reaction (RT-PCR). The protein expression of FN, Col-I HO-1 and ET-1 were analyzed by enzyme-linked immunosorbent assay or immunofluorescence method. RESULTS: The expression of protein and mRNA of FN and Col-I were attenuated by Danshensu in both dose-dependent and time-dependent manner. The mRNA and protein levels of ET-1 were decreased, and the mRNA and protein levels of HO-1 increased in the Danshensu groups in a dose-dependent manner compared with the high glucose group. The expression of ET-1 and HO-1 showed little difference in a time gradient of danshensu(P>0.05). CONCLUSION Danshensu can protect HPMCs through inhibiting the expression of FN and Col-I induced by high glucose, which is related to the suppression of oxidative stress.
Cell Line ; Cells, Cultured ; Collagen Type I ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Epithelial Cells ; metabolism ; Fibronectins ; metabolism ; Glucose ; pharmacology ; Humans ; Lactates ; pharmacology ; Peritoneum ; cytology

OBJECTIVE: To investigate the role of phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) inducing epithelial mesenchymal transition in human peritoneal mesothelial cells (HPMC). METHODS: Primary HPMC was harvested from human omental tissue and maintained under defined in vitro conditions. The expression of p-GSK-3beta and total GSK-3beta in HMPC was detected by Western blot after incubation with different concentrations (0, 5, 10, 20, and 40 mmol/L)of LiCl at different time points (0, 1, 3, 6, and 12 h). The protein expression of E-cadherin and alpha-SMA was also examined after treatment with 20 mmol/L LiCl according to different time courses. The intracellular distribution and expression of alpha-SMA were determined by indirect immunofluorescence. RESULTS: LiCl stimulated phosphorylation of GSK-3beta and the effect was time-dependent and concentration-dependent to limited extent (P<0.05). The expression of alpha-SMA increased (P<0.05) and the expression of E-cadherin decreased significantly (P<0.05) after 24 h stimulation by 20 mmol/L LiCl. The indirect immunoflurescence showed that the expression of alpha-SMA in HPMC increased significantly after 24 h incubation with 20 mmol/L LiCl. CONCLUSION The phosphorylation of GSK-3beta leads HMPC to epithelial mesenchymal transition and provides new clue for the treatment of peritoneal fibrosis.
Actins ; metabolism ; Cadherins ; metabolism ; Epithelial Cells ; cytology ; drug effects ; Epithelial-Mesenchymal Transition ; drug effects ; Glycogen Synthase Kinase 3 ; metabolism ; Glycogen Synthase Kinase 3 beta ; Humans ; Lithium Chloride ; pharmacology ; Mesoderm ; cytology ; drug effects ; Peritoneum ; cytology ; Phosphorylation