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...
Polycystic ovarian syndrome (PCOS) is a low grade inflammatory disease characterized by hyperandrogenemia and chronic anovulation. C-reactive protein (CRP), released by adipocytes, plays a key role in PCOS. Apis mellifera honeybee venom (HBV) contains a variety of biologically active components with various pharmaceutical properties. This study was designed to assess the possibility of HBV application as an anti-inflammatory therapeutic agent. To induce PCOS, 1 mg/100 g body weight estradiol valerate (EV) was subcutaneously (SC) injected into eight-week-old rats. After 60 days, 0.5 mg/kg HBV was administered SC for 14 consecutive days, and the results of PCOS treatment were investigated. Rats were then anesthetized with chloroform, and their ovaries and livers were surgically removed to determine histomorphometrical changes. Testosterone and 17-β-estradiol were detected by chemiluminescence immunoassay. In order to detect serum CRP, ELISA kit was used in three groups of EV-induced PCOS, HBV-treated PCOS and control animals. Thickness of the theca layer, number of cysts and the level of serum CRP significantly decreased in HBV group in comparison with PCOS group. Moreover, corpus luteum, as a sign of ovulation, was observed in HBV-treated ovaries which were absent in PCOS group. Our results suggest that the beneficial effect of HBV may be mediated through its inhibitory effect on serum CRP levels.
Purpose: HIF-1α has critical roles in formation of Tumor microenvironment by regulating genes involved in angiogenesis and anaerobic respiration. TME fuels tumors growth and metastasis and presents therapy with several challenges. Therefore, we aimed to investigate if Melittin disrupts HIF-1α signaling pathway in breast adenocarcinoma cell line MDA-MB-231.Methods: breast adenocarcinoma cell line MDA-MB-231 was cultured in presence of different doses of Melittin and MTT assay was carried out to measure Melittin's cytotoxic. Cells were exposed to 5% C 2 to mimic hypoxic conditions and Melittin. Western blot was used to measure HIF-1α protein levels. Gene expression analysis was performed using real-time PCR to measure relative mRNA abundance of genes involved in tumor microenvironment formation.Findings: Our results revealed that Melittin effectively inhibits HIF-1α at transcriptional and translation/post-translational level. HIF-1α protein and mRNA level was signi cantly decreased in Melittin-treated groups. It is found that inhibition of HIF-1α by Melittin is through downregulation of NFκB gene expression. Furthermore, gene expression analysis showed a downregulation in VEGFA and LDHA expression due to inhibition of HIF-1α protein by Melittin. In addition, cell toxicity assay showed that Melittin inhibits the growth of MDA-MB-231 cell line through activation of extrinsic and intrinsic apoptotic pathways by upregulating TNF and BAX expression.Conclusions: Melittin suppresses the expression of genes responsible for formation of TME physiological hallmarks by suppressing HIF-1α signaling pathway. Our results suggest that Melittin can modulate tumor microenvironment by inhibition of VEGFA and LDHA.
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.
Introduction. Honey bee venom (HBV) has various biological activities such as the inhibitory effect on several types of cancer. Cisplatin is an old and potent drug to treat most of the cancers. Our aim in the present study was to determine antimutagenic and cytotoxic effects of HBV on mammary carcinoma, exclusively and in combination with cisplatin. Methods. In this study, 4T1 cell line was cultured in RPMI-1640 with 10% fetal bovine serum (FBS), at 37°C in humidified CO2 incubator. The cell viabilities were examined by the MTT assay. Also, HBV was screened for its antimutagenic activity via the Ames test. The results were assessed by SPSS software version 19 and one-way ANOVA method considering p<0.05 level of significance. Results. The results showed that 6 mg/ml of HBV, 20 μg/ml of cisplatin, and 6 mg/ml HBV with 10 μg/ml cisplatin could induce approximately 50% of 4T1 cell death. The concentration 7 mg/ml of HBV with of 62.76% inhibitory rate showed the highest antimutagenic activity in comparison with other treatment groups. Conclusions. The MTT assay demonstrated that HBV and cisplatin could cause cell death in a dose-dependent manner. The cytotoxic effect of cisplatin also promoted by HBV. Ames test outcomes indicated that HBV could act as a significant mutagenic agent. The antimutagenic activity of HBV was increased considerably in the presence of S9 mix. Therefore, our findings have revealed that HBV can enhance the cytotoxic effect of cisplatin drug and its cancer-preventing effects.
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