Background: Having low-grade chronic inflammation state symptoms such as elevated C-reactive protein and interleukin-6 play a crucial role in polycystic ovary syndrome (PCOS). Green tea has antiinflammatory properties. This research evaluates the effect of green tea on inflammatory indexes. Adult Wistar rats were exposed to subcutaneous administration of estradiol valerate for PCOS induction. PCOS rats were divided into control and experimental groups received intraperitoneal injection green tea extract daily. Animals were anesthesia with chloroform. Ovary and serum were taken to measure the inflammatory markes using ELISA kits and Histomorphometric studies. The data were analyzed using One-Way ANOVA with significance level P<0.05.Results: The results indicated the significant reduction in inflammatory markers and significant changes follicular layers thickness in the treatment group as compared with control.Disscoution: it can be concluded that having anti-inflammatory substances, green tea is effective in symptoms of this syndrome and metabolic syndrome.Keywords: Polycystic ovary syndrome, Wistar rat, green tea extract, inflammation, ELISA. BackgroundCytokines play a major role in response to the inflammatory stimuli and tissue damages. Interleukin (IL) -6 (20-30 kD aglycoprotein) is a pleiotropic cytokine, which is mainly produced by immune system and different types of adipose tissue, hepatocytes, and ovarian follicular granulosa [1]. Interleukin receptors are made of two sets, including GP-130 and il-6r. Interleukin-6 is on 7p21 chromosome. International Journal of Cellular & Molecular Biotechnology 2014 (2014 [1][2][3][4][5][6][7][8][9][10][11][12] Available online at www.ispacs.com/ijcmb is basically regulated by Beta Kappa core factor (NK-kb) and interleukin IL-6 causes stimulus, regulates synthesis of acute phase protein, activates axis of hypothalamus -pituitary and disorder in signal transduction of glucose through changing activity of serine -threonine kinases. Interleukin-6 plays a key role in the pathogenesis of chronic inflammation, insulin resistance, and CV diseases [2]. CRP is a member of pentraxinsfamily. As the most sensitive inflammatory indices, CRP plays an important role in immune response. In human, CRP gene lies on 1q21 to 1q23 chromosomes. CRP protein is produced by liver and it is almost the strongest inflammatory marker, as its increase is responsible for inflammation. Appearance of CRP is considered as a strong predicator for metabolic abnormality. This substance is produced in liver and intimal of vessels. Despite CRP's inflammatory role, using different mechanisms, such as producing nitric oxide (NO), increasing molecules adhesion, and changing absorption of low-density lipoprotein (LDL) by macrophages, it is able to damage vessels. The increase of this protein (as an independent predicator of CV risk) increases damages to CV system 2 -5 times. Its content is mainly regulated by some cytokines, especially 1L6 [2]. PCOS is a reproduction abnormality together with a metab...

In early stages of development, the laminated structure of cerebral cortex is organized by proliferative, morphogenetic, and migratory processes. In these stages, cells within the ependymal lining of neural tube are thought to secrete embryonic cerebrospinal fluid (eCSF). As the neural tube closes, the choroid plexuses (CPs) secrete proteins such as growth factors, cytokines and morphogenes into the eCSF. The apical neuroepithelium is bathed with this fluid which plays regulatory roles in cortical cell proliferation, differentiation, and maintenance. Because of the eCSF protein contents and their impacts on neurogenesis, we focused on the effect of eCSF growth factors and their changes during brain development. Bibliographic databases including PubMed, Scopus and Google Scholar were searched between years 1990 to 2013 for the keywords "Cerebrospinal fluid" and "Neurogenesis". In the first step, 200 articles were found, after elimination of duplicates or irrelevant papers 49 papers were selected and reviewed.

BackgroundPolycystic ovarian syndrome (PCOS) is a low-grade inflammatory disease characterized by hyperandrogenemia, hirsutism, chronic anovulation and vascular disorder. Interleukin-6 (IL-6), cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) are triggered by inflammatory stimuli and lead to angiogenesis and pathogenesis of the ovary. Honeybee venom (HBV) contains an array of biologically active components possessing various pharmaceutical properties. This study was designed to assess the possibility of HBV application as an anti-inflammatory therapeutic agent to suppress levels of the main inflammatory mediators IL-6, COX-2 and VEGF.To induce PCOS, 1 mg of estradiol valerate (EV) per 100 g of body weight was subcutaneously (SC) injected into eight-week-old rats. After 60 days, 0.5 mg/kg of HBV was administered Intraperitoneal (IP) for 14 consecutive days, and the results of PCOS treatment were investigated. Rats were then anesthetized with CO2, and the ovaries were surgically removed. Serum IL-6 was detected by the ELISA kit. Immunoexpression of COX-2 and VEGF were examined in three groups: EV-induced PCOS, HBV-treated PCOS and control animals.ResultsThickness of theca layer, number and diameter of cysts and levels of IL-6 significantly decreased in HBV group relative to PCOS group. The immunohistochemical analysis showed an increase in COX-2 and VEGF expression in PCOS group whereas HBV-treated rats presented weak and irregular immunostaining.ConclusionsOur results suggest that the beneficial effect of HBV may be mediated through its inhibitory effect on serum IL-6 level and ovarian COX-2 and VEGF expression.

Background: Aquaporins (AQPs) are water channels that play a key role in water transport in many epithelia. Recent studies have shown that AQP1, located in the apical membrane of choroid plexus cells, has an important role in cerebrospinal fluid (CSF) production. However, the mechanism of water transport through the basolateral membrane of choroid plexus (CP) cells is yet to be determined. Objectives: In this study, the expression and localization of AQP1, AQP4 and AQP5 in the rat lateral ventricle CP were investigated by immunocytochemistry, western analysis and flowcytometry. Materials and Methods: Choroidal epithelial cells of the lateral ventricle in Wistar rats were isolated and grown in Dulbecco's Modified Eagle's medium (DMEM) supplement, which was refreshed every two days. After five days, the expression patterns of AQP1, AQP4 and AQP5 were determined by immunoblotting, immuncytochemistry and flowcytometry. Results: The immunocytochemistry data revealed the expression of AQP1 and AQP4 in the membrane and the cytoplasmof AP cells, respectively. Through western analysis, the AQP1 antibody detected two bands of approximately 27 and 32 kDa. A single peptide of 29 kDa was recognized by the AQP4 antibody. Quantitative flowcytometry revealed CP cells exhibiting a high level of AQP1 and AQP4 proteins (95.39% and 92.21%, respectively). According to immunocytochemistry, AQP5 is weakly expressed in the cytoplasm of CP cells. Anti-AQP5 antibody recognized a pale band of approximately28 kDa by western analysis. Conclusions: These observations suggested that AQP4 may have an important role in CSF secretion; however, expression of AQP4 or AQP5 was not detected in the cell membrane. Thus, how water crosses the basolateral membrane of CP cells remains to be determined.

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