Protective effect of metformin on a rat model of lipopolysaccharide‐induced preeclampsia

Hu, Jilin; Zhang, Jinman; Zhu, Baosheng

doi:10.1111/fcp.12501

Cited by 33 publications

(24 citation statements)

References 61 publications

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“…Apart from type 2 diabetes, metformin is also used to prevent or delay the onset of diabetes in subjects at high risk for this disease [21,22]. Prediabetes is an intermediate state of hyperglycemia with glycemic parameters above normal but below the diabetes threshold, reflecting the presence of either, or both, impaired fasting glucose and impaired glucose tolerance [23,24].…”

Section: Introductionmentioning

confidence: 99%

Plasma gonadotropin levels in metformin‐treated men with prediabetes: a non‐randomized, uncontrolled pilot study

Krysiak

Szkróbka

Bednarska-Czerwińska³

2020

Fundamemntal Clinical Pharma

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Metformin was found to reduce elevated, but not normal, thyrotropin and prolactin levels. This non‐randomized, uncontrolled pilot study investigated hypothalamic–pituitary–testicular axis activity in men with primary hypogonadism receiving metformin. The study population included 29 men with prediabetes, 10 of whom had been diagnosed with primary hypogonadism. Throughout the study, the participants were treated with metformin (2.55–3 g daily). Glucose homeostasis markers (fasting glucose, glycated hemoglobin, and HOMA1‐IR), as well as circulating levels of follicle‐stimulating hormone (FSH), luteinizing hormone (LH), testosterone, thyrotropin, prolactin, estradiol, and creatinine, were assessed at the beginning of the study and 16 weeks later. Both groups differed in baseline gonadotropin and testosterone levels. Fasting glucose, glycated hemoglobin, and HOMA1‐IR were lower after than before metformin treatment. The changes in fasting glucose and HOMA1‐IR were more pronounced in hypogonadal men than in subjects with testosterone levels within the reference range. Only in hypogonadal men, plasma concentrations of FSH and LH were lower at the end than at the beginning of the study. Levels of the remaining hormones remained unchanged throughout the study period. The reduction in FSH and LH levels correlated with their baseline levels and with the changes in HOMA1‐IR. The results of our study suggest that metformin may decrease FSH and LH levels in men with hypergonadotropic hypogonadism.

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Section: Introductionmentioning

confidence: 99%

Plasma gonadotropin levels in metformin‐treated men with prediabetes: a non‐randomized, uncontrolled pilot study

Krysiak

Szkróbka

Bednarska-Czerwińska³

2020

Fundamemntal Clinical Pharma

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“…Microglia are encephalic cells that are local macrophages of the central nervous system and play an essential role in cerebral immune function. Microglial inflammation induced pro‐inflammatory cytokines and pro‐inflammatory enzymes expression , thus resulting in inflammation‐induced neuronal cell death. Recently, increased intracellular glycolysis was indicated to participate in LPS‐mediated immune cells and microglia inflammation .…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine attenuates LPS‐mediated BV2 microglia cells inflammation via inhibition of glycolysis

Meng

Duan

et al. 2019

Fundamemntal Clinical Pharma

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Meng and Yu Equal contributes. A B S T R A C TMicroglia inflammation induces pro-inflammatory cytokines and pro-inflammatory enzymes expression, thus leading to inflammation-mediated neuronal cell death. Increased intracellular glycolysis participates in LPS-mediated microglia inflammation. Dexmedetomidine exhibits neuroprotective effects in some situations. In this study, we mainly focused on whether and how dexmedetomidine inhibits LPS-mediated cellular glycolysis and inflammation in BV2 cells. LPS induced pro-inflammatory cytokines and pro-inflammatory enzymes expression, and increased glycolysis capacity in BV2 cells. Moreover, inhibition of glycolysis by 2DG attenuated LPS-induced pro-inflammatory cytokines and pro-inflammatory enzymes expression. Moreover, LPS upregulated hypoxia-inducible factor 1a (HIF1a) expression and decreased sirt1 expression. Dexmedetomidine counteracted these effects induced by LPS. Further, 2-methoxyestradiol, a HIF1a inhibitor, could inhibit LPSmediated glycolysis and inflammation in BV2 cells, which was similar to the effects of dexmedetomidine. In addition, these effects of dexmedetomidine could be reversed by EX527, a sirt1 inhibitor. The present study indicated that dexmedetomidine, via upregulation of sirt1 expression, inhibited HIF-1a expression and glycolysis, thus reducing LPS-mediated inflammation in BV2 cells.

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“…This resulted in a normalization of blood pressure, reduced proteinuria, improvement in fetal growth, and decreased stillbirth frequency. The authors concluded that metformin is beneficial to the PE-like rat model by protecting placentas from injury; thus, it could be an attractive agent for PE prevention and/or treatment [123]. It has been reported that the decrease in IL-27, TNF-α, and IL-6 expression in vivo (in both preeclamptic rat models and trophoblast cells) was the result of H19 inhibition by metformin in a dose-dependent manner [124].…”

Section: Impact On Preeclampsia Pathophysiologymentioning

confidence: 99%

Prevention of Hypertensive Disorders of Pregnancy—Is There a Place for Metformin?

Poniedziałek‐Czajkowska

Mierzyński

Dłuski

et al. 2021

JCM

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The possibility of prophylaxis of hypertensive disorders of pregnancy (HDPs) such as preeclampsia (PE) and pregnancy-induced hypertension is of interest due to the unpredictable course of these diseases and the risks they carry for both mother and fetus. It has been proven that their development is associated with the presence of the placenta, and the processes that initiate it begin at the time of the abnormal invasion of the trophoblast in early pregnancy. The ideal HDP prophylaxis should alleviate the influence of risk factors and, at the same time, promote physiological trophoblast invasion and maintain the physiologic endothelium function without any harm to both mother and fetus. So far, aspirin is the only effective and recommended pharmacological agent for the prevention of HDPs in high-risk groups. Metformin is a hypoglycemic drug with a proven protective effect on the cardiovascular system. Respecting the anti-inflammatory properties of metformin and its favorable impact on the endothelium, it seems to be an interesting option for HDP prophylaxis. The results of previous studies on such use of metformin are ambiguous, although they indicate that in a certain group of pregnant women, it might be effective in preventing hypertensive complications. The aim of this study is to present the possibility of metformin in the prevention of hypertensive disorders of pregnancy with respect to its impact on the pathogenic elements of development

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Protective effect of metformin on a rat model of lipopolysaccharide‐induced preeclampsia

Cited by 33 publications

References 61 publications

Plasma gonadotropin levels in metformin‐treated men with prediabetes: a non‐randomized, uncontrolled pilot study

Plasma gonadotropin levels in metformin‐treated men with prediabetes: a non‐randomized, uncontrolled pilot study

Dexmedetomidine attenuates LPS‐mediated BV2 microglia cells inflammation via inhibition of glycolysis

Prevention of Hypertensive Disorders of Pregnancy—Is There a Place for Metformin?

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