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Fig. 7 | Journal of Biomedical Science

Fig. 7

From: Activation of TrkB/Akt signaling by a TrkB receptor agonist improves long-term histological and functional outcomes in experimental intracerebral hemorrhage

Fig. 7

The schematic diagram indicates the potential mechanisms of TrkB activation-induced neuroprotection in ICH mice. As summarized in Fig. 7, we found that treatment with 7,8-DHF promoted neuronal survival and reduced apoptosis, attenuated brain tissue damage, cerebral edema and behavioral deficits following ICH. These effects were related to increase TrkB and subsequently Akt activation in neurons, and enhancing Ask-1 and FOXO-1 phosphorylation after ICH. 7,8-DHF also increased short-term BDNF expression after ICH. Our findings suggest that pharmacological enhancement of TrkB signaling by 7,8-DHF could be a potential strategy for the management of ICH. DHF: 7,8-dihydroxyflavone

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Journal of Biomedical Science

ISSN: 1423-0127