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Effect of alpha‐lipoic acid and myoinositol on endometrial inflammasome from recurrent pregnancy loss women
Author(s) -
Di Nicuolo Fiorella,
D'Ippolito Silvia,
Castellani Roberta,
Rossi Esther Diana,
Masciullo Valeria,
Specchia Monia,
Mariani Marco,
Pontecorvi Alfredo,
Scambia Giovanni,
Di Simone Nicoletta
Publication year - 2019
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.13153
Subject(s) - inflammasome , endometrium , western blot , pregnancy , medicine , alpha (finance) , immunohistochemistry , endocrinology , biology , inflammation , biochemistry , surgery , construct validity , genetics , patient satisfaction , gene
Problem A significant increased expression/activation of one of the most well‐characterized inflammasomes, the NAcht leucine‐rich‐repeat protein‐3 (NALP‐3), in the endometrium from idiopathic recurrent pregnancy loss women (RPL) has been previously found by our research group. We therefore, suggested this event as being one of the molecular mechanisms altering endometrial inflammatory status during early pregnancy. In the present research, we attempt to investigate whether molecules with anti‐inflammatory activity, alpha‐lipoic acid (ALA), and/or myoinositol affect the endometrial NALP‐3 expression and activation. Method of study Women with a history of idiopathic RPL (n = 30) were included in the study and compared to a control group (n = 15). Endometrial tissues were collected by hysteroscopy during the mid‐luteal phase. RPL women underwent a three‐month prescription of tablets containing ALA plus myoinositol (Sinopol ® ). After treatment, hysteroscopic biopsies were repeated in RPL patients. Inflammasome expression was evaluated by immunohistochemical and Western blot analysis. NALP‐3 activation was studied by quantifying the secretion of both caspase‐1 and interleukin (IL)‐1ß and IL‐18 through ELISA. In ex vivo experiments, the effects of each molecule on endometrial inflammasome were studied. Results Sinopol ® significantly reduced the RPL endometrial inflammasome expression and activation. ALA, but not myoinositol, significantly reduced the endometrial inflammasome expression and activity. Conclusion Our data suggest a role for ALA on RPL inflammasome. Understanding the mechanisms involved in RPL and the observation that specific molecules are able to interfere with such complex at the endometrium might provide new rational design approaches to a personalized evaluation of endometrial status and, ultimately, a targeted medicine.