Neurotropin® alleviates hippocampal neuron damage through a HIF‐1α/MAPK pathway

Abstract

Neurotropin® exhibited a potent neuroprotective effect on inhibiting Aβ-induced oxidative damage and alleviating Aβ deposition in hippocampus via modulation of HIF-1α/MAPK signaling pathway.

The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer’s Disease in APPSwe/PS1dE9 Mice

“…Activation of c-Jun N-terminal kinase (JNK) has been reported in APPSwe/PS1dE9 mice to induce long-term synaptic toxicity and cognition impairment (Fang et al, 2017;Liang et al, 2019). Vanadium was demonstrated to decrease phosphorylation of JNK (p-JNK) and thus reduce JNK activation (Wang et al, 2015;Kim and Kim, 2019).…”

Geniposide attenuates Aβ25–35-induced neurotoxicity via the TLR4/NF-κB pathway in HT22 cells

“…As shown in Fig. 6, exposure to Ab [25][26][27][28][29][30][31][32][33][34][35] ( Though recent researches conjecture that Ab is an immune stress responsed to brain infection. Ab is a savior in the brain tissue rather than a killer.…”

“…30 Moreover, recent studies have shown that Ab 25-35 can signicantly promote the nuclear translocation of p65 subunit leading to p65 activation and over-expression of inammatory mediators including TNF-a, IL-1, COX-2 and iNOS. [31][32][33] Hence, the nuclear transport of NF-kB/p65 was observed by immunouorescence test under the uorescent microscope to discriminate the effect of geniposide treatment on nuclear transport of NF-kB/p65 induced by Ab [25][26][27][28][29][30][31][32][33][34][35] . Fig.…”

“…9 shows that NF-kB/p65 mainly appears in the cytoplasm of HT22 cells in control group. On the contrary, Ab 25-35 evidently promotes NF-kB/p65 to transfer into nucleus representing NF-kB/p65 is activated by Ab [25][26][27][28][29][30][31][32][33][34][35] . The effect of Ab 25-35 -induced nuclear transport of NF-kB/p65 is reversed when HT22 cells are treated with geniposide (160 mM) and TAK 242 (1 mM).…”

“…Although the mechanism between the inammatory response and the pathogenesis of AD is still unclear, it is certain that neuroinammation induced by Ab plays a critical role in promoting the progression of AD. Ab [25][26][27][28][29][30][31][32][33][34][35] , a shorter fragment stems from amyloid precursor protein, performs the similar neurotoxic function to Ab and it is the main responsibility for neurotoxicity of Ab. 9 Toll-like receptors (TLRs), the Ab-recognized pattern recognition receptors, play central roles not only in the beginning of macrophages and immune reactions, but also in the occurrence of inammatory diseases, for example AD.…”