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Effect of Coenzyme Q 10 on Th1/Th2 Paradigm in Females with Idiopathic Recurrent Pregnancy Loss
Author(s) -
Talukdar Ayantika,
Sharma Kandala Aparna,
Rai Reeta,
Deka Dipika,
Rao Donthamsetty Nageshwara
Publication year - 2015
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12376
Subject(s) - peripheral blood mononuclear cell , immune system , proinflammatory cytokine , cytokine , medicine , endocrinology , immunology , reactive oxygen species , flow cytometry , andrology , oxidative stress , pregnancy , in vitro , biology , inflammation , biochemistry , genetics
Problem Recurrent pregnancy loss is characterized by predominant T h1‐type immunity and increased reactive oxygen species. Low levels of C oenzyme Q 10 are found in the plasma of RPL as compared to healthy pregnant females. Our aim was to investigate whether in vitro supplementation of PBMC s from such females with C o Q 10 could change the observed T h1 bias. Method of study PBMC s were isolated from 20 RPL pregnant and non‐pregnant females and 16 healthy pregnant females and incubated with C o Q 10 in in vitro conditions. Phenotyping of T h1, T h2, and T h17 cells was performed by flow cytometry. Cytokine levels were determined by ELISA . Results PBMC s treated with C o Q 10 showed significantly decreased percentage of T h1 cells ( P  < 0.005) in pregnant females with history of RPL than in the untreated ones. Also, levels of IFN‐γ and TNF‐α were significantly decreased in the culture supernatant of treated PBMCs from RPL. DCFDA staining showed significantly reduced production of ROS in the treated PBMC s in RPL females. Conclusion C o Q 10 was effective in maintaining the immune homeostasis by reducing the proportion of IFN ‐γ‐producing T cells and proinflammatory cytokine levels in the RPL pregnant females. This property could be attributed to the capability of C o Q 10 in reducing oxidative stress by decreasing ROS production.

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