Relationship of Estrogen Intestinal Microbiological Axis of Estrogen with Metabolic Defects in SD Rat Model of Polycystic Ovary Syndrome Induced by DHEA
Relationship of Estrogen Intestinal Microbiological Axis of Estrogen with Metabolic Defects in SD Rat Model of Polycystic Ovary Syndrome Induced by DHEA
Jiahua Peng1,2, Shiyao Hua3* and Qian Wu4
ABSTRACT
The objective was to study the relationship between the intestinal microbiological axis of estrogen and metabolic defects in SD rat model of polycystic ovary syndrome (PCOS) induced by DHEA, and to explore the possible mechanism. Forty rats were randomly divided into four group, the model groups each of 10 the control group, the DHEA group (low dose, 15 μg/kg/d) and the DHEA group (high dose, 30 μg/kg/d). DHEA subcutaneous injection was used to construct the PCOS model of the polycystic ovary syndrome (PCOS) model of rats. The general condition of rats (body weight, ovary weight) and ovarian tissue pathology changes were observed. The changes in content of testosterone (T), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were detected. The fasting blood glucose, serum insulin and insulin sensitive index changes were analyzed. The RT-PCR method was used to detect ovarian tissue TNF alpha and the level of IL-6 gene expression; Western blot was used to detect the changes in the expression levels of IKKβ and NF-κB protein expression. The results of fasting blood glucose and serum insulin test showed that DHEA could significantly reduce fasting blood glucose and insulin levels and improve insulin sensitivity index, and the effect was more obvious in the high-dose group. The above results indicated that DHEA could regulate the intestinal microbial level of rats, and further regulate the sugar metabolism process of rats by increasing the serum estrogen level through the estrogen-microbial axis. RT-PCR and Western Blot analysis showed that the expression of TNF-α, IL-6, IKKβ, NF-κB increased significantly after the establishment of the model; after the administration of DHEA, the levels of TNF-α, IL-6, IKKβ, NF-κB were down-regulated, and the difference was statistically significant compared with the model group (P<0.05). It is concluded that DHEA could regulate estrogen levels in rats through the estrogen-intestinal microbiological axis, thereby improving insulin resistance and reducing blood glucose levels. The mechanism of DHEA may be related to the inhibition of the expression of inflammatory factors and the inhibition of NF-κB nuclear transposition through the IKK/NF-κB signaling pathway.
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