Expression of CD44 and NANOG in epithelial ovarian cancer and its clin-ical significance / 中国病理生理杂志

AIM:To investigate the expression of CD44 and transcription factor NANOG in epithelial ovarian cancer(EOC)and its clinical significance.METHODS:The expression of CD44 and NANOG in EOC and benign ovarian tumor tissues were detected by immunohistochemical method.The correlation between the expression of CD 44 and NANOG in EOC was analyzed.The expression of CD44 and NANOG in ovarian cancer cell line SKOV3 after treatment with cisplatin at different concentrations were detected by Western blot.RESULTS:The positive expression rates of CD44 and NANOG in EOC were significantly higher than those in benign ovarian tumor tissues(P<0.01).In EOC,positive correlation was observed between the expression of CD 44 and NANOG(r=0.346,P<0.01).The positive expression rate of CD44 was associated with clinical stage and lymphatic metastasis(P<0.05), and had no relationship with age, histological grade, pathological types and the location of tumors.The positive expression rate of NANOG was associated with clinical stage and histological grade(P<0.05),and had no relationship with age,lymphatic metastasis,pathological types and the location of tumors.Increased expression of CD44 and NANOG were detected in ovarian cancer cell line SKOV 3 after treatment with cisplatin(P<0.05).CONCLUSION:The over-expression of CD44 and NANOG are associated with the occurrence and development of EOC.The expression of cancer stem cells marker CD 44 and the pluripotent gene product pertaining to em-bryonic stem cells NANOG are increased in cisplatin-induced SKOV3 cells.Cancer stem cells and the expression of stem-ness-related gene may well be the underlying pathogenesis that promotes the onset, progression, and chemotherapy resist-ance of EOC.

Metformin versus metformin plus rosiglitazone in women with polycystic ovary syndrome / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hyperinsulinemia and insulin resistance are present in the majority of women with polycystic ovary syndrome (PCOS). Both metformin and rosiglitazone can improve the ovulation and endocrine disorders of the patients. How about the combination of the two? It is rarely reported. This study aimed to compare the therapeutic efficacy of metformin versus metformin plus rosiglitazone in patients with PCOS.</p><p><b>METHODS</b>Fifty-eight women with PCOS were randomly assigned to two groups. Metformin group (29) was treated with metformin mono-therapy and metformin plus rosiglitazone group (29) was treated with metformin plus rosiglitazone for 6 months. Treatment was discontinued once pregnancy was diagnosed.</p><p><b>RESULTS</b>Fasting insulin, postprandial insulin, the homeostatic model assessment of insulin resistance (HOMA-IR), luteinizing hormone (LH), triglyceride, lower density cholesterol and testosterone level decreased significantly in both groups (P < 0.05). Metformin plus rosiglitazone had a better effect than metformin mono-therapy. Body mass index decreased by 7.8% in metformin group while no significant change in metformin plus rosiglitazone group. There were eight pregnancies, six in metformin plus rosiglitazone group (one abortion) and two in metformin group. There was no congenital anomaly at birth and seven infants developed well at one year's follow-up.</p><p><b>CONCLUSIONS</b>Metformin can improve insulin resistance and imbalance of endocrine hormones. Metformin plus rosiglitazone has a more pronounced therapeutic effect and achieved more pregnancies than mono-therapy with metformin. The use of metformin and rosiglitazone before pregnancy has no obvious side effect on the development of the infants. Our study might suggest that metformin is the better choice in PCOS patients with serious obese and rosiglitazone plus metformin would be more effective in patients with severe insulin resistance or those do not respond to metformin.</p>

Effects of benazepril on renal function and kidney expression of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 in diabetic rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Excessive deposition of extracellular matrix (ECM) in the kidney is the hallmark of diabetic nephropathy. Increased matrix synthesis has been well documented but the effects of diabetes on degradative pathways, particularly in the in vivo setting. The renal protective effect of these pathways on matrix accumulation has not been fully elucidated. The present study was undertaken to investigate the activity of matrix metalloproteinase-2 (MMP-2), the expression of MMP-2 and tissue inhibitor of metalloproteinase-2 (TIMP-2) in kidney tissues of diabetic rats, and to explore the degradative pathway of type IV collagen (IV-C) and the renal protective effects of ACE inhibition-benazepril.</p><p><b>METHODS</b>Twenty-four healthy male Wistar rats were divided randomly into normal control group (NC group), untreated diabetes mellitus group (DM group), and diabetes mellitus group treated with benazepril (DL group). The rat model of diabetes mellitus was induced by intraperitoneal injection of streptozocin (60 mg/kg). After the establishment of DM model, benazepril (10 mg.kg(-1).d(-1)) was given to the DL group for 12 weeks, and the same volume of water was given to the other two groups. At the end of 12 weeks, renal function was evaluated with 24-hour urinary protein (Upro), clearance of creatinine (Ccr), and blood urea nitrogen (BUN). MMP-2 activity was determined by gelatin zymography. The levels of MMP-2, TIMP-2 and collagen IV (IV-C) protein in the kidney tissue were assessed by immunohistochemistry. The gene expression of MMP-2 and TIMP-2 was measured by reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The levels of BUN, Upro and Ccr in the DM group were higher than those in the NC group. In the DM group, the mRNA, enzymatic activity and proteins of MMP-2 decreased, but the expressions of IV-C and TIMP-2 increased. All diabetes-associated changes in renal function and MMP/TIMP were attenuated after benazepril treatment with reduced IV-C accumulation.</p><p><b>CONCLUSIONS</b>The changes of MMP-2 and TIMP-2 expressions in kidney tissues of diabetes rats may contribute to the occurrence and progression of diabetic nephropathy. Benazepril could exert protective effects on diabetic nephropathy, owing to the upregulation of MMP-2 and downregulation of TIMP-2 expressions, which further inhibits the excessive deposition of extracellular matrix in the glomerulus.</p>