Objective To investigate the changes of serum and urinary adiponectin (ADPN) levels and insulin resis-tance (IR) states in patients with chronic kidney disease (CKD), and to explore their relationship thereof. Methods A total of 487 patients with CKD stages 2-5 were enrolled in this study, and 30 healthy subjects were served as control group. The se-rum ADPN levels in urine samples were examined by ELISA. The level of fasting insulin (FINS) was detected by radioimmu-noassay. Blood routine test, liver and kidney functions, blood glucose, serum lipids, 24 h urinary protein excretion and endoge-nous creatinine clearance rate (Ccr) and body mass index (BMI) were observed and calculated. The differences of ADPN lev-els in serum and urine samples and homeostasis model assessment for insulin resistance (Homa-IR) were compared between groups. Results The serum and urine ADPN levels and Homa-IR were higher in CKD patients than those of controls (P＜0.05). With the decline in renal function, the ADPN and Homa-IR levels were increased gradually (P＜0.05). The value of se-rum ADPN was significantly higher in patients with CKD stages 3-5 and high Homa-IR. The ADPN levels and Homa-IR were positively related to lipid parameters and 24 h urinary protein, and negatively correlated with hemoglobin and serum al-bumin in patients with CKD (P ＜ 0.05). Conclusion CKD patients had higher ADPN level and more significant IR. The ADPN and IR were correlated with serum lipids, hemoglobin, albumin and urinary protein. Dynamic monitor of ADPN level may have clinical significance in judging metabolic disorders in CKD patients.

We examined the effects of marine fish oil, which is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA),in 22 patients with chronic renal failure (CRF). At 8 weeks treatment,marine fish oil led to decreases in both plasma triglyceride ( -24. 7%) and cholesterol (-14. 8%),and increases in high density lipoprotein and the ratio of apolipoprotein Al/apolipoprotein B. Meanwhile, the endogeneous creatinine clearance was raised by 39. 6%,and the increasing rate of serum creatinine level was slowed down. We conclude that supplementation of co-3 polyunsaturated fatty acids can effectively improve the abnormalities of lipids metabolism in CRF. It is beneficial to retardation of progression of CRF,and to reduction of the risk of cardiovascular complications. We hold that marine fish oil can be used as a supplementary drug in the treatment of CRF.

We find that there is a correlation among thesize of ventricular septal defect (VSD) (X_2), PaO_2(X_3), V. /V. (X_7) and pulmonary systolic pressure(Y_1), diastolic pressure (Y_2), mean pressure (Y_3)by multivariate stepwise regression analysis, andso there are their parameters in the regression e-quations. The regression equations are Y_1 = 13. 24+ 0. 22X_2 - 0. 09X_3 + 0. 14X_7; Y_2 = 0. 65 + 0. 24X_2+ 0. 12X_7; Y_3 = 3. 54+ 0. 17X_2 + 0. 16X_7. But thecourse of the disease, ∑9 leads QRS dimension,R. /R., L. /L. are non-dominant factors, and sothere are not their parameters in the regression e-quation. The above-mentioned equations mayavoid the patients. with mild, moderate pulmonaryhypertension to have invasive examination, and re-duce its complications.

Ovarian cancer bears the highest mortality in gynecologic cancer, and its 5-year survival rate is about 30%. Although 70% to 80% ovarian cancer is epithelial origin, increasing evidence indicates that reciprocal interactions between tumor cells and various types of stromal cells also play important roles in driving ovarian tumor progression and that these stromal cells represent attractive therapeutic targets. This review discusses the biological signiifcance of the cross-talk between ovarian cancer cells and three major types of stromal cells (endothelial cells, ifbroblasts and macrophages) and the development of new-generation therapies that target the ovarian tumor micro-environment.

OBJECTIVE:To discuss about the internationalized management of Chinese medicine enterprises in our country METHODS:To analyse the internationalization of Chinese medicine enterprises in the aspects of necessity,possibility and the essentials for implementation RESULTS & CONCLUSION:Facing the new management environment brought by development of international natural drug market,globalization of economy and China joining WTO,the Chinese medicine enterprises in our country should conform to the trend of the times,grasp opportunity,face the challenge Then they could survive and develop

Objective To investigate the effects and mechanisms of prostaglandin E2 receptor subtype 3 (EP3) on transforming growth factor β1 (TGF-β1)-induced mouse mesangial cells damage. Methods Primary mouse mesangial cells were separated and cultured. Three siRNAs were synthesized and transfected into mesangial cells for silencing EP3 by LipofectamineTM 2000 and the best one was chosen. MCs were grouped into: (1)control group; (2)TGF-β1 (10 μg/L) group; (3)NC-siRNA plus TGF-β1 (10 μg/L) group; (4) EP3-siRNA group; (5)EP3-siRNA plus TGF-β1 (10 μg/L). Then the proliferation of MCs was evaluated by CCK-8 assay. The expression of PGE2 and cAMP in cell supernatant were detected by ELISA. The mRNA and protein expression of fibronectin (FN), connective tissue growth factor (CTGF), cyclooxygenase-2 (COX2), membrane-bound prostaglandin E2 synthase 1 (mPGES1) were detected by real - time quantitative PCR and Western blotting. The phosphorylation of p38 MAPK and ERK1/2 was decected by Western blotting. Results Compared with control group, the cell proliferation induced by TGF-β1 was increased (P<0.05), the expression of PGE2 and cAMP were improved, mRNA and protein expression of FN, CTGF, COX2 and mPGES1 were up-regulated (all P<0.05). Compared with TGF-β1 group, the cell proliferation in EP3-siRNA plus TGF-β1 group was reduced, the expression of FN, CTGF, COX2 and mPGES1 mRNA and protein were downregulated (all P<0.05), the phosphorylation of ERK1/2, p38 MAPK were also declined (P<0.05). Conclusion EP3-siRNA may reduce TGF-β1-induced cell damage through upregulating the expression of cAMP, repressing the activity of ERK1/2 and p38 MAPK, inhibiting the expression of COX2 mPGES1 and PGE2 by feedback, then decreased the expression of FN and CTGF.

Objective To study the effects of simvastatin on proliferation and apoptosis in rat mesangial cells in vitro, and to investigate the signal pathways involved in apoptosis induced by simvastatin. Methods Cultured mesangial cells were treated with simvastatin. Proliferation of mesangial cells was examined by MTT assay. Simvastatin-treated apoptotic mesangial cells were observed by electron microscopy. Propidium iodide (PI) staining and flow cytometry were employed for quantitative measurement of apoptosis. Caspase-3 activation was determined by CaspGLOW Green Caspase-3 Staining Kit. Results (1)Simvastatin significantly inhibited proliferation of mesangial cells compared with control (P

Objective To investigate the effects of antisense p21 oligodeoxynucleotide (p21 ASODN) on the expression of p21 protein and extracellular matrix in cultured human glomerular mesangial cells (HGMC) under high glucose medium. Methods HGMCs were transfected with 50 nmol/L or 100 nmol/L p21 ASODN or scrambled control oligodeoxynucleotide (SCODN) using lipofectamine 2000. After incubation under normal (5.5 mmol/L) or high (30 mmol/L) glucose media and different times, HGMCs lysates were collected and the expression of p21, fibronectin and laminin was examined by Western blot. The secretion of fibronectin and laminin by HGMCs in supernatants of culture media was also detected with EOSA. Results High glucose media significantly stimulated the expression of p21, increased the syntheses and secretion of fibronectin and laminin in cultured HGMCs in a time-dependent manner. Transfection of HGMCs with p21 ASODN not only decreased p21 protein level caused by high glucose media, but also attenuated the expression and secretion of fibronectin and laminin in supematants of HGMCs lysates and culture media. Meanwhile, SCODN had no significant effects on the expression of p21, fibronectin and laminin. Conclusions High glucose promotes the expression of p21 , fibronectin and laminin in cultured HGMCs. Transfection of HGMCs with p21 ASODN can decrease p21 protein level caused by high glucose media, and attenuate the expression of fibronectin and laminin in supematants of HGMCs lysates and culture media. Modulation of p21 expression in HGMCs may work as an effective way to mitigate the progression of diabetic nephropathy.

ObjectiveTo investigate the expression and activity of Rho-associated kinase 1 (ROCK1) in renal tissues of uninephrectomized diabetic rats,and to explore the possible mechanism of renal protection of spironolactone.Methods The model rats were established by a single intraperitoneal injection of streptozotocin(STZ) after uninephrectomy and randomly divided into sham operation group(N),uninephrectomized control group?,uninephrectomized diabetic group (D),and spironolactone treated group (S).Four and 8 weeks later,biochemical indexes and renal morphology were detected.Expressions of ROCK1 and connect tissue growth factor (CTGF) were examined by immunohistochemistry and real-time PCR.Protein expression of p-MYPT1 was examined by Westem blotting.Results After 4 and 8 weeks,compared with group N and C,blood glucose,systolic blood pressure,24-h urinary protein,kidney weight/body weight (KWI) were significantly increased (P＜0.01),and extracellular matrix proliferation and basement membrane thickening were found in group D.After 8 weeks in group D,Alb significantly decreased and Scr significantly increased (P＜0.05).In group D,protein and mRNA expression of ROCK1 and CTGF increased significantly and protein expression of p-MYPT1 increased significantly as well with time.Treatment with spironolactone could partially reverse those changes. ConclusionsExpression and activity of ROCK1increase in renal tissues of uninephrectomized diabetic rats and are positively correlated with the expression of CTGF.Spironolactone can protect the kidney of diabetic rats in early stage probably through decreasing the expression of ROCK1,CTGF and inhibiting the activation of ROCK1.

Objective To investigate the effects of triptolide on proliferation,apoptosis and the changes of Ski,Smad3,Smad7 and collagen type I(ColI) in cultured rat mesangial cells induced by transforming growth factor (TGF)-β1.Methods Cultured HBZY-1 rat mesangial cells were divided into 5 groups:(1)normal control group; (2)TGF-β1 group (10 μg/L); (3)-(5)triptolide (0.4,2,10 μg/L)+TGF-β1 (10 μg/L) groups.The cell proliferation was detected by MTT.Apoptosis of mesangial cells was detected by TUNEL assay.The expressions of Ski,Smad3,Smad7 mRNA were examined by real-time quantitative PCR.The expressions of Ski,Smad3,Smad7 and ColI protein were detected by Western blotting.The localizations of Ski and Smad3 protein were detected by laser confocal fluorescence microscope.Results Compared with the normal control,TGF-β1 (10 μg/L) significantly stimulated mesangial cells proliferation,while decreased apoptosis.The mRNA and protein expressions of Ski,Smad7,Smad3 and ColI protein expression in TGF-β1 group were increased (P ＞0.05).In comparison with TGF-β1 group,triptolide could significantly inhibit TGF-β1-induced mesangial cells proliferation in dose-dependent manner,and promote the apoptosis of mesangial cells.In TGF-β1 group,mRNA and protein expresscons of Ski and Smad7 were increased (P＜0.05),Smad3 mRNA and protein were decreased (P ＞0.05),and ColI protein was decreased (P＜0.01).In comparison with TGF-β1 group,fluorescence intensity of Ski,Smad3 proteins was significantly increased in cytoplasm,while decreased in nucleus.Conclusions Triptolide can inhibit TGF-β1-induced mesangial cells proliferation through regulating the expressions of Ski,Smad7 mRNA and protein,inhibiting Ski.Smad7 translocation to the nucleus,and down-regulating Smad3 mRNA and protein expression.Triptolide can promote apoptosis of mesangial cells.