Serum S100B indicates brain edema formation and predicts long-term neurological outcomes in rat transient middle cerebral artery occlusion model

Neuroprotective effect of Artemisia absinthium L. on focal ischemia and reperfusion-induced cerebral injury

“…Present investigations revealed that pre-treatment with EAA offered effective protection against neuronal damage induced by MCAO as EAA markedly reduced the infarct volume in dose dependent manner (Fig. 1), in harmony with other studies (Walberer et al, 2006;Tanaka et al, 2007).…”

Serum S100B is a useful surrogate marker for long-term outcomes in photochemically-induced thrombotic stroke rat models

“…These reports support the observation in the current study of serum S100B kinetics peaking 48 h after the onset of PIT stroke. The serum S100B kinetics observed in the current study is similar to those observed in stroke patients (Büttner et al, 1997;Wunderlich et al, 1999;Herrmann et al, 2000;Foerch et al, 2004) and in another rat stroke model involving intraluminal suture methods (Tanaka et al, 2007).…”

“…Serum S100B levels were significantly higher in the "severe" group at 24 and 48 h than in the "moderate" group. One of our previous studies had detected no serum S100B in naïve rats of equivalent age and strain (Tanaka et al, 2007).…”

Electroacupuncture-Like Stimulation at the Baihui (GV20) and Dazhui (GV14) Acupoints Protects Rats against Subacute-Phase Cerebral Ischemia-Reperfusion Injuries by Reducing S100B-Mediated Neurotoxicity

“…Increasing evidence has shown that an increase in the synthesis of S100B by activated astrocytes in the periinfarct area is positively associated with the severity of delayed infarct expansion and neurological deficits in models of middle cerebral artery occlusion (MCAo) [1], [4], whereas S100B inhibitors exert potential neuroprotective effects against cerebral ischemic injuries [5], [6]. Thus, the S100B is an effective biomarker of the severity of infarction and the extent of brain edema, as shown by previous clinical [7] and experimental stroke [8] studies. During the subacute phase of cerebral ischemia, astrocytes release S100B, which interacts with the receptor for advanced glycation end products (RAGE) to stimulate the microglial secretion of proinflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), by activating nuclear factor-κB (NF-κB).…”