Protein expression profiling of rat uteruses with primary dysmenorrhea syndrome

Abstract

Purpose The aim of this study was to investigate differentially expressed proteins (DEPs) and their functions in the uteruses of primary dysmenorrhea (PD) rats by using label-free quantitative proteomics analysis.Methods The PD rat model was induced by injecting both estradiol benzoate and oxytocin. Twenty rats were equally divided into two groups: a control group (normal rats), a PD model group (PD rats). Writhing scores and serum levels of Prostaglandin E2 (PGE2) and Prostaglandin F2α (PGF2α) were used to evaluate the success of the rat PD model. The DEPs were identi ed and analyzed by label-free quantitative proteomics and bioinformatics analyses.Results A total of 276 DEPs were identi ed, including 119 up-regulated DEPs and 157 down-regulated DEPs. Bioinformatics revealed that the DEPs were mainly associated with 'protein binding', 'metabolism', 'signal conduction' and 'focal adhesion'. The proteomic ndings were veri ed by western blot analysis, which con rmed that myosin light chain kinase (MLCK), heat shock protein 90 AB1 (HSP90AB1), apolipoprotein A1 (Apoa1), p38 MAP kinase, c-Jun N-terminal kinase (JNK), and extracellular signalrelated kinase 1/2 (ERK1/2) were signi cantly differentially expressed in between the control and PD samples.Conclusions These results provide a deeper understanding the molecular pathogenesis of PD. The DEPs found in the present study may provide new ideas for further study of the mechanism of PD and aid the search for biomarkers for early diagnosis and treatment.

To explore the mechanism of acupoint application in the treatment of primary dysmenorrhea by 16S rDNA sequencing and metabolomics

“…Cortisol, a hormone type on the Steroid hormone biosynthesis pathway, is significantly reduced in patients with dysmenorrhea and is negatively correlated with the duration of symptoms ( 58 ). Estradiol on the Prostate cancer pathway is generally used as an inducing factor for the manufacture of dysmenorrhea animal models, and its concentration is positively correlated with the risk of dysmenorrhea ( 59 ). Biotin on the Biotin metabolism pathway has a strong analgesic effect and is closely related to the occurrence of dysmenorrhea ( 60 ).…”

The mechanism of ginger and its processed products in the treatment of estradiol valerate coupled with oxytocin-induced dysmenorrhea in mice via regulating the TRP ion channel-mediated ERK1/2/NF-κB signaling pathway

“…43,44 Activated TRPV1 and TRPM8 can increase the intracellular Ca 2+ content while the activated Ca 2+ /CaMKII can subsequently elevate the expression of downstream ERK 1/2 to mediate an oxytocin signal and regulate the production of inflammatory cytokines. [45][46][47] Phosphorylated ERK can affect the phosphorylation of IκB α , an important indicator of the activation of the NF-κB pathway, which in turn can induce the aberrant activation of some key proteins, such as p65. 48 Phosphorylated NF-κB can induce the expression of COX-2 and limit the rate of transformation of arachidonic acid to PGs.…”

Consumption of Artificial Sweetener Acesulfame Potassium Increases Preterm Risk and Uterine Contraction with Calcium Influx Increased via Myosin Light Chain Kinase–Myosin Light Chain 20 Related Signaling Pathway

“…[27] Primary dysmenorrhea rat also show a significantly increase in JNK protein expression. [28] To understand the Ace K-induced signaling transduction, we used a JNK inhibitor SP600125 to block the signaling pathway. The results indicated that SP600125 pretreatments could partially block the Ace K effect on uterine contraction.…”