Neuro endocrinology letters · 2024
Practical viewpoints on ethical questions and dilemmas in schema therapy.
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Cheng Xiumei, Cao Xinyi, Yang Yichun, Wang Lingxiao, Yang Yuxuan, Pan Yunjian, Zheng Yongliang, Wei Churong, Luo Yougen
Аннотация
OBJECTIVE: Methylmercuric chloride (MMC) has neurotoxicity, while hydrogen sulfide (H2S) has shown inhibitory properties against nerve damage induced by various factors. The study aimed to investigate the impact of H2S on MMC-induced learning and memory impairment in mice and to explore the underlying mechanisms.
METHODS: A mouse model of learning and memory impairment was established by MMC gavage, and sodium hydrosulfide (NaHS) was used as an H2S donor for intervention. Cell viability and live/dead cell ratio in HT22 neuronal cells were assessed by CCK-8 assay and Calcein/PI staining, respectively. The Morris water maze test was performed to evaluate the learning and memory abilities of mice. Western blotting was utilized to determine protein expressions of BDNF and TrkB. The effects of H2S on MMC-induced learning and memory impairment were investigated based on the BDNF/TrkB pathways.
RESULTS: (1) MMC treatment decreased cell viability and reduced the ratio of live cells in HT22 cells, while H2S reversed these changes. (2) MMC prolonged escape latency, decreased platform crossing frequency, and reduced quadrant distance percentage of the platform in the Morris water maze test, while H2S reversed the above changes. (3)MMC downregulated BDNF and TrkB expression levels, while H2S suppressed these changes induced by MMC. (4)Treatment with 7, 8-DHF (a TrkB agonist) significantly attenuated MMC-induced prolonged escape latency and reduced platform crossing frequency.
CONCLUSIONS: Our findings demonstrated that H2S ameliorated learning memory deficits in mice by reversing the inhibitory effects of MMC on BDNF/TrkB signaling pathway.
METHODS: A mouse model of learning and memory impairment was established by MMC gavage, and sodium hydrosulfide (NaHS) was used as an H2S donor for intervention. Cell viability and live/dead cell ratio in HT22 neuronal cells were assessed by CCK-8 assay and Calcein/PI staining, respectively. The Morris water maze test was performed to evaluate the learning and memory abilities of mice. Western blotting was utilized to determine protein expressions of BDNF and TrkB. The effects of H2S on MMC-induced learning and memory impairment were investigated based on the BDNF/TrkB pathways.
RESULTS: (1) MMC treatment decreased cell viability and reduced the ratio of live cells in HT22 cells, while H2S reversed these changes. (2) MMC prolonged escape latency, decreased platform crossing frequency, and reduced quadrant distance percentage of the platform in the Morris water maze test, while H2S reversed the above changes. (3)MMC downregulated BDNF and TrkB expression levels, while H2S suppressed these changes induced by MMC. (4)Treatment with 7, 8-DHF (a TrkB agonist) significantly attenuated MMC-induced prolonged escape latency and reduced platform crossing frequency.
CONCLUSIONS: Our findings demonstrated that H2S ameliorated learning memory deficits in mice by reversing the inhibitory effects of MMC on BDNF/TrkB signaling pathway.