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Effect of fish oil and telmisartan on dehydroepiandrosterone?induced polycystic ovarian syndrome in rats: The role of oxidative stress, transforming growth factor beta?1, and nuclear factor kappa B

ABSTRACT: Abstract Our aim was to explore the effect of telmisartan and/or fish oil on dehydroepiandrosterone (DHEA)?induced PCOS in rats. Sixty female rats were divided into six equal groups as follows: Control; DHEA?induced PCOS; DHEA + Telmisartan; DHEA + Fish oil; DHEA + Carboxymethyl cellulose; and DHEA + Telmisartan +Fish oil group. Plasma sex hormones, anthropometric measurements, and the glycemic indices were measured. Tissue oxidative stress parameters and the proinflammatory cytokines were assessed. The ovaries were subjected to histopathological and electron microscopic examination. Telmisartan and/or fish oil induced significant improvement of insulin resistance with amelioration of oxidative stress and inflammation compared to PCOS group. Also, telmisartan and/or fish oil restored the hormonal levels and the anthropometric measurements to the normal values. This was significant with telmisartan/fish oil combination compared to the use of each of these agents alone. In conclusion, this combination may represent a promising hope for amelioration of PCOS. We investigated the effect of fish oil and/or telmisartan on PCOS. Fish oil and/or telmisartan restored the hormonal balance, produced antioxidant and anti?inflammatory effects, and attenuated insulin resistance. Fish oil and/or telmisartan combination was better than each of these drugs alone.

SUBMITTER: Kabel A

PROVIDER: S-EPMC7500795 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND:Previous studies have shown that chronic inflammation and oxidative stress may play an important role in the pathophysiology of polycystic ovary syndrome (PCOS), and glutamine (Gln) have showed the anti-inflammatory and antioxidant properties. So the aim of this study is to investigate the effect of glutamine supplementation on PCOS rats. METHODS:Female Sprague-Dawley rats were randomly assigned into four groups (n =?10 /group), control group, PCOS group, PCOS+?0.5?g/kg Gln group and PCOS+?1.0?g/kg Gln group. All the PCOS rats were administrated with 6?mg/100?g dehydroepiandrosterone (DHEA) for 20 consecutive days, all the PCOS+Gln groups were intraperitoneal injected glutamine twice in the next morning after the last DHEA injection. All the samples were collected 12?h after the last administration. Ovarian histological examinations were analyzed and the concentration of serum hormone, inflammatory and oxidative stress factors were measured. RESULTS:There was no obvious ovarian histological change among the PCOS group and PCOS+Gln groups. All the detected inflammation factors [C-reactive protein, interleukin (IL)-6, IL-18, tumor necrosis factor] showed significantly higher in all the PCOS groups compared to the control group (P <?0.01), and were significantly decreased with the supplementation of 0.5?g/kg glutamine (P <?0.01). Concentrations of superoxide dismutase were significantly lower in all the PCOS groups (P <?0.01) compared to the control group, and increased significantly with the supplementation of 0.5?g/kg glutamine (P <?0.01). Serum concentrations of malondialdehyde, nitric oxide synthase and nitric oxide were significantly higher in PCOS group (P <?0.01) compared with the control group, and significantly decreased to the comparative levels of control group with supplementation of 0.5?g/kg glutamine (P <?0.01). CONCLUSION:There is low-grade inflammation and oxidative stress in DHEA-induced PCOS rats. The supplementation of 0.5?g/kg glutamine could effectively ameliorate the inflammation and oxidative stress conditions of PCOS.

Project description:BackgroundFish oil supplements that are rich in omega-3 long-chain polyunsaturated fatty acids (n-3 PUFAs). PUFAs are among the most widely-used dietary supplements globally, and millions of people consume them regularly. There have always been public concerns that these products should be guaranteed to be safe and of good quality, especially as these types of fish oil supplements are extremely susceptible to oxidative degradation.ObjectivesThe aim of the current study is to investigate and examine the oxidation status of dietary supplements containing fish oils and to identify important factors related to the oxidation status of such supplements available in the United Arab Emirates (UAE).MethodsA total of 44 fish oil supplements were analysed in this study. For each product, the oxidative parameters peroxide value (PV), anisidine value (AV), and total oxidation (TOTOX) were calculated, and comparisons were made with the guidelines supplied by the Global Organization for EPA and DHA Omega-3s (GOED). Median values for each of the above oxidative parameters were tested using the Kruskal-Wallis and Mann-Whitney U tests. P values < 0.05 were chosen as the statistically significant boundary.ResultsThe estimate for the average PV value was 6.4 with a 95% confidence interval (CI) [4.2-8.7] compared to the maximum allowable limit of 5 meq/kg. The estimate for the average P-AV was 11 with a 95% CI [7.8-14.2] compared to the maximum allowable limit of 20. The estimate for the average TOTOX value was 23.8 meq/kg with a 95% CI [17.4-30.3] compared to the maximum allowable limit of 26 according to the GOED standards.ConclusionThis research shows that most, although not all, of the fish oil supplements tested are compliant with the GOED oxidative quality standards. Nevertheless, it is clear that there should be a high level of inspection and control regarding authenticity, purity, quality, and safety in the processes of production and supply of dietary supplements containing fish oils.

Project description:Persistent high-risk human papillomavirus (HPV) infection is the major causal factor in cervical and other anogenital cancers. Because there are currently no therapeutics capable of preventing neoplastic progression of HPV infections, understanding the mechanisms of HPV-mediated persistence, including immune evasion, is a major research priority. The multifunctional growth factor transforming growth factor beta (TGF?) has been shown to inhibit expression of early viral transcripts from cells harboring integrated HPV genomes or cells infected with retroviruses expressing HPV oncoproteins. However, the mechanism of TGF?-induced inhibition has not been fully defined. In this study, we have observed a previously uncharacterized ability of TGF? to repress the differentiation-induced upregulation of late HPV16 gene expression. In addition, interferon kappa (IFN-?), a keratinocyte-specific, constitutively expressed cytokine suppressed by differentiation, can be transcriptionally induced by TGF?1. TGF?-mediated IFN-? transcription only occurs in cells containing HPV16, and this is due to TGF?1-mediated reversal of HPV-induced methylation of the IFN-? promoter through active DNA demethylation mediated by thymine DNA glycosylase (TDG). This novel interaction between growth factor and innate immune signaling may shed light on the mechanisms of HPV persistence and how the virus manipulates both immune and growth factor signaling to promote its life cycle.IMPORTANCE Persistent infection by high-risk HPVs is the primary risk factor for development of HPV-induced cancers. Persistence involves viral evasion of the immune response, including the IFN response. HPV is also known to suppress TGF? signaling, which inhibits viral gene expression. Here, we show that the TGF? and IFN pathways are interrelated in the context of HPV16 infection through the upregulation of IFN-? by TGF?. The ability of TGF? to induce IFN-? promoter demethylation and transcriptional activation provides a new explanation for why HPV has evolved mechanisms to inhibit TGF? in infected cells.

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Effect of fish oil and telmisartan on dehydroepiandrosterone?induced polycystic ovarian syndrome in rats: The role of oxidative stress, transforming growth factor beta?1, and nuclear factor kappa B

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