A Comparative Proteomic Analysis to Explore the Influencing Factors on Endometritis Using LC-MS/MS.

The inflammatory system activated by uterine infection is associated with decreased fertility. Diseases can be detected in advance by identifying biomarkers of several uterine diseases. Escherichia coli is one of the most frequent bacteria that is involved in pathogenic processes in dairy goats. The purpose of this study was to investigate the effect of endotoxin on protein expression in goat endometrial epithelial cells. In this study, the LC-MS/MS approach was employed to investigate the proteome profile of goat endometrial epithelial cells. A total of 1180 proteins were identified in the goat Endometrial Epithelial Cells and LPS-treated goat Endometrial Epithelial Cell groups, of which, 313 differentially expressed proteins were accurately screened. The proteomic results were independently verified by WB, TEM and IF techniques, and the same conclusion was obtained. To conclude, this model is suitable for the further study of infertility caused by endometrial damage caused by endotoxin. These findings may provide useful information for the prevention and treatment of endometritis.

Proteomic analysis of uterine lavage fluid of dairy cows at different time after delivery by mass spectrometry.

Endometritis is a common disease in the reproductive system, which is the infection and inflammation of the endometrium. In severe cases, it can affect the myometrium and adversely affect the subsequent fertility of dairy cows. We used a mass spectrometry-based technique to compare proteomics of uterine lavage fluid between healthy cows and cows with cytological endometritis classified according to 100-day postpartum pregnancy results and diagnosis result. The uterine lavage fluid of dairy cows collected at 15 and 30 days after delivery was analyzed. 15 days postpartum, we identified a total of 1129 proteins in the control and cytological endometritis (CEM) groups. Among them, 160 proteins were accurately screened out. 30 days postpartum, we identified a total of 846 proteins in the control and cytological endometritis (CEM) groups. Among them, 186 proteins were accurately cytological endometritis (CEM). Endometritis is a costly reproductive disease in lactating cows, which needs to be diagnosed in time. Using proteomics method based on gel mass spectrometry, we compared the proteome of uterine lavage fluid of dairy cows with and without cytological endometritis to characterize the changes of proteomic characteristics associated with postpartum uterine disease. To provide reference for clinical application and basic research.

Schisandrin Protects against Norepinephrine-Induced Myocardial Hypertrophic Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.

Aims. Heart failure is closely associated with norepinephrine-(NE-) induced cardiomyocyte hypertrophy. Schisandrin is derived from the traditional Chinese medicine Schisandra; it has a variety of pharmacological activities, and the mechanism of schisandrin-mediated protection of the cardiovascular system is not clear. Main Methods. NE was used to establish a cardiomyocyte hypertrophy model to explore the mechanism of action of schisandrin. An MTT assay was used for cell viability; Hoechst fluorescence staining was used to observe the cell morphology and calculate the apoptosis rate. The cell surface area was measured and the protein to DNA ratio was calculated, changes in mitochondrial membrane potential were detected, and the degree of hypertrophic cell damage was evaluated. WB, QRT-PCR, and immunofluorescence were used to qualitatively, quantitatively, and quantitatively detect apoptotic proteins in the JAK2/STAT3 signaling pathway. Key Findings. In the NE-induced model, schisandrin treatment reduced the apoptosis rate of cardiomyocytes, increased the ratio of the cell surface area to cardiomyocyte protein/DNA, and also, increased the membrane potential of the mitochondria. The expression of both JAK2 and STAT3 was downregulated, and the BAX/Bcl-2 ratio was significantly reduced. In conclusion, schisandrin may protect against NE-induced cardiomyocyte hypertrophy by inhibiting the JAK2/STAT3 signaling pathway and reducing cardiomyocyte apoptosis.