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Table 2 TLRs postconditionings and effects

From: Function and mechanism of toll-like receptors in cerebral ischemic tolerance: from preconditioning to treatment

Animal Model Postconditioning time/approach TLR/ischemia Results/mechanism Author References
Mice MCAO, ischemia 2 h CCA 10-s ligation, subsequently 30-s open, a total of 3 cycles Ischemic postconditioning Decrease brain infarction volume and improve neurological function. Activate AKT signaling pathway Gao X [92]
Mice MCAO, 60-min ischemia, 24-h reperfusion 30 min/systemic injection TLR2, Pam3CSK4 Decrease brain infarction volume and improve neurological function. Activate TLR2/PI3K/Akt signaling pathway Lu C [65]
Mice MCAO, 60-min ischemia, 24-h reperfusion 30 min/IP TLR3 poly-IC Decrease brain infarction and prevention of Fas/FADD interaction Zhang X [67]
Mice MCAO, 60-min ischemia, 48-h reperfusion 3 h/IP TLR3 poly-IC Decrease brain infarction volume and improve neurological function. Downregulate TLR4 signaling pathway by TLR3 Wang PF [90]
Mice MCAO, 60-min ischemia, 24-h reperfusion 15 min/IP TLR9 CpG-ODN Decrease brain infarction and activation of PI3K/Akt Signaling Lu C [78]
  1. MCAO: middle cerebral artery occlusion; IP: intraperitoneal injection; CCA: common carotid artery TLR: toll-like receptor; Poly-IC: polycytidylic acid; FADD: Fas-Associated protein with Death Domain; CpG-ODN: CpG-motif oligodeoxynucleotide. MCAO, 60-min ischemia, 24-h reperfusion: the mice was employed MCAO (cerebral ischemia) 60 min followed by reperfusion 24 h. 3 h/IP: Mice were injected intraperitoneally with TLRs ligand 3 h after cerebral ischemia.