Baicalin Protects Vascular Tight Junctions in Piglets During Glaesserella parasuis Infection

Abstract

Glaesserella parasuis (G. parasuis) can cause Glässer's disease and severely affect swine industry worldwide. This study is an attempt to address the issue of the capability of G. parasuis to damage the vascular barrier and the effects of baicalin on vascular tight junctions (TJ) in order to investigate the interactions between the pathogen and the porcine vascular endothelium. Piglets were challenged with G. parasuis and treated with or without baicalin. The expressions of vascular TJ genes were examined using RT-PCR. The distribution patterns of TJ proteins were detected by immunofluorescence. The involved signaling pathways were determined by Western blot assays on related proteins. G. parasuis can downregulate TJ expression and disrupt the distribution of TJ proteins. Baicalin can alleviate the downregulation of vascular TJ mRNA, maintain the distribution, and prevent the abnormalities of TJ. These results provide ample evidence that baicalin has the capacity to protect vascular TJ damaged by G. parasuis through inhibiting PKC and MLCK/MLC pathway activation. As a result, baicalin is a promising candidate for application as a natural agent for the prevention and control of G. parasuis infection.

Baicalin alleviates endometrial inflammatory injury through regulation of tight junction proteins

“…25 Baicalin exhibits ameliorative effects on barrier damage in the brain, peritoneum, and vessels. 26–28 Here, we found that baicalin prevented endometrial barrier integrity by altering the redistribution of TJ proteins via autophagy. Pharmacological and genetic modification of autophagy affects the baicalin-induced redistribution of TJ proteins with LPS treatment (Fig.…”

“…8 In addition, the protective effects of baicalin on tight junctions during inflammatory injury were reported in previous publications. 9,10 However, the preventive effects of baicalin on the endometrial barrier remain unknown.…”

Quercetin Protects Blood–Brain Barrier Integrity via the PI3K/Akt/Erk Signaling Pathway in a Mouse Model of Meningitis Induced by Glaesserella parasuis

“…Increased BBB permeability is usually associated with changes in ZO-1, Occludin, and Claudin-5 [ 46 ].The expression of TJ proteins (ZO-1, Occludin, and Claudin-5) is significantly reduced in LPS-stimulated human microvascular endothelial cells (HBMECs), resulting in BBB dysfunction [ 47 ]. Previous studies have reported that G. parasuis can affect the vascular endothelial barrier by downregulating vascular TJ expression and disrupting the distribution of TJ proteins (ZO-1, Occludin, Claudin-5, and JAM-1) [ 48 ]. It has been reported that G. parasuis could disrupt intercellular junctions and facilitate bacterial translocation across the tracheal epithelium by activating the p38/MAPK pathway [ 49 ].…”

Baicalin-aluminum complex on the regulation of IPEC-1 infected with enterotoxigenic Escherichia coli

“…Pig diarrhea caused ETEC is often associated with the innate immune response and impaired intestinal barrier function [ [31] , [32] , [33] ]. Consistent with our previous studies, the results have shown that baicalin could inhibit activation of nuclear factor-kappa B and NLRP3 inflammasome signaling pathways in piglet mononuclear phagocytes and porcine aortic vascular endothelial cells of piglets during G. parasuis infection or LPS stimulation [ 15 , 34 , 35 ], and protect peritoneal/vascular tight junctions damaged with inhibition of the activation of protein kinase C and myosin light chain kinase/myosin light chain signaling pathway induced by G. parasuis [ 19 , 36 ]. This effect may be attributed to protection of the BA complex against pig diarrhea, which promotes protection of porcine intestinal cells and maintains the epithelial barrier and immunity function.…”