文獻引用抗體：bs-2558R

Anti-EGFRvIII pAb

bs-0028R ; Anti-GSK-3 Beta pAb; WB

bs-0061R ; Anti-beta-Actin (Loading Control) pAb; WB

bs-14519R ; Anti-phospho-eIF2B epsilon (Ser539) pAb; WB

bs-14533R ;  Anti-eIF2B epsilon pAb; WB

bs-17330R ; Anti-hnRNP A1 pAb; WB

bs-20611R ; Anti-PI 3 Kinase p85 alpha pAb; WB

bs-23217R ; Anti-NFKB p65 pAb; WB

bsm-33278M ; Mouse Anti-AKT mAb; WB

bs-0295P-HRP ; Rabbit IgG/HRP; WB

bs-0805R ; Anti-CD56 pAb

bs-0832R ; Anti-MICA pAb

bs-0938R ; Anti-NKG2D pAb

bs-1214R ; Anti-TRAIL pAb

bs-2411R ; Anti-NKG2A pAb

bs-2420R ; Anti-NCR2 pAb

bs-2569R ; Anti-CD226 pAb

bs-6028R ; Anti-CD16 pAb

bs-6874R ; Anti-Catalase pAb

bs-20399R ; Anti-HIF-1 Alpha pAb

bs-41214R ; Anti-NCR1 pAb

bs-0295G-AF594 ; Goat Anti-Rabbit IgG H&L/Alexa Fluor 594

作者單位：北京理工大學生命科學學院

文獻引用抗體：bs-6313R 

Anti-4 Hydroxynonenal pAb

文獻引用抗體：bs-6313R 

Anti-Biglycan pAb; WB

作者單位：復旦大學華山醫院骨科

摘要：Background

Toll-like receptor 4 (TLR4) participates in the initiation of neuroinflammation in various neurological diseases, including central nervous system injuries. NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated microglial pyroptosis is crucial for the inflammatory response during secondary spinal cord injury (SCI). However, the underlying mechanism by which TLR4 regulates NLRP3 inflammasome activation and microglial pyroptosis after SCI remains uncertain.

Methods

We established an in vivo mouse model of SCI using TLR4-knockout (TLR4-KO) and wild-type (WT) mice. The levels of pyroptosis, tissue damage and neurological function recovery were evaluated in the three groups (Sham, SCI, SCI-TLR4-KO)...

文獻引用抗體：

bs-2994R 

Anti-IRF7 pAb; WB

bsm-34028M 

Mouse Anti-ADGRE1 (F4/80) mAb; IHC

摘要：Diarrheal disease is a common health problem with complex causality. Although diarrhea is accompanied by disturbances in microbial diversity, how gut microbes are involved in the occurrence of diarrhea remains largely unknown. Here, using a pig model of post-weaning stress-induced diarrhea, we aim to elucidate and enrich the mechanistic basis of diarrhea. We found significant alterations in fecal microbiome, their metabolites, and microRNAs levels in piglets with diarrhea. Specifically, loss of ssc-miRNA-425-5p and ssc-miRNA-423-3p, which inhibit the gene expression of fumarate reductase (frd) in Prevotella genus, caused succinate accumulation in piglets, which resulted in diarrhea. Single-cell RNA sequencing indicated impaired epithelial function and increased immune response in the colon of piglet with diarrhea. Notably, the accumulated succinate increased colonic fluid secretion by regulating transepithelial Cl-secretion in the epithelial cells. Meanwhile, succinate promoted colonic inflammatory responses by activating MyD88-dependent TLR4 signaling in the macrophages. Overall, our findings expand the mechanistic basis of diarrhea and suggest that colonic accumulation of microbiota-produced succinate caused by loss of miRNAs leads to diarrhea in weanling piglets.