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.

Serum Metabolomics Revealed the Differential Metabolic Pathway in Calves with Severe Clinical Diarrhea Symptoms.

The complex etiology, higher morbidity and mortality, poor prognosis, and expensive cost of calf diarrhea have made it a catastrophic disease in the dairy industry. This study aims to assess the biomarkers in calves with diarrhea and to predict the biomarkers related to the pathway. As subjects, nine calves with diarrhea and nine healthy calves were enrolled, according to strict enrollment criteria. The serum metabolites were detected by a liquid chromatographic tandem mass spectrometry (LC-MS/MS), and then analyzed by online multivariate statistical analysis software to further screen the biomarkers. In addition, the biomarkers involved in the metabolic pathways of calves with diarrhea and healthy calves were analyzed. In the serum of calves with diarrhea, nine biomarkers were found to which several biomarkers exhibited a certain relation. Moreover, these biomarkers were involved in important metabolic pathways, including protein digestion and absorption, ABC transporters, aminoacyl-tRNA biosynthesis, mineral absorption, and fatty acid biosynthesis. All these findings suggested that the imbalance of these markers was closely related to the occurrence and development of calf diarrhea. The targeted regulation of metabolic pathways involved in these biomarkers may facilitate the diagnosis, treatment, and discussion of the mechanism of calf diarrhea.

Differences in the intestinal microbiota between uninfected piglets and piglets infected with porcine epidemic diarrhea virus.

Porcine epidemic diarrhea, a disastrous gastrointestinal disease, causes great financial losses due to its high infectivity, morbidity and mortality in suckling piglets despite the development and application of various vaccines. In this study, high-throughput sequencing was used to explore differences in the intestinal microbiota between uninfected piglets and piglets infected with porcine epidemic diarrhea virus (PEDV). The results revealed that the small intestinal microbiota of suckling piglets infected with PEDV showed low diversity and was dominated by Proteobacteria (49.1%). Additionally, the composition of the small intestinal microbiota of sucking piglets infected with PEDV showed marked differences from that of the uninfected piglets. Some of the taxa showing differences in abundance between uninfected piglets and piglets infected with PEDV were associated with cellular transport and catabolism, energy metabolism, the biosynthesis of other secondary metabolites, and amino acid metabolism as determined through the prediction of microbial function based on the bacterial 16S rRNA gene. Therefore, adjusting the intestinal microbiota might be a promising method for the prevention or treatment of PEDV.

Immunomodulatory activity in vitro and in vivo of polysaccharide from Potentilla anserina.

The polysaccharide (PAP) from Potentilla anserina was evaluated for modulating effects by using mouse peritoneal macrophage and the immunosuppressed-model cyclophosphamide-induced. Phagocytotic and mononuclear phagocytic system function assays showed that PAP stimulated the phagocytosis of phagocyte. Splenocyte proliferation assay showed that PAP acted the effect combining Con A or LPS in splenocyte proliferation. The parameters detected showed that PAP increased thymus and spleen indices, the levels of LDH and ACP in the spleen, and IL-10 and IFN-γ in serum in immunosuppressed mice. The results suggest that PAP is involved in immunomodulatory effects leading to the exploration for PAP as a potential immunostimulant.