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10.1177/1759091415578711

http://scihub22266oqcxt.onion/10.1177/1759091415578711
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C4397212!4397212!25873304
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suck abstract from ncbi


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pmid25873304      ASN+Neuro 2015 ; 7 (2): ä
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  • Cystathionine ?-Synthase Inhibition Is a Potential Therapeutic Approach to Treatment of Ischemic Injury #MMPMID25873304
  • Chan SJ; Chai C; Lim TW; Yamamoto M; Lo EH; Lai MKP; Wong PTH
  • ASN Neuro 2015[Mar]; 7 (2): ä PMID25873304show ga
  • Hydrogen sulfide (H2S) has been reported to exacerbate stroke outcome in experimental models. Cystathionine ?-synthase (CBS) has been implicated as the predominant H2S-producing enzyme in central nervous system. When SH-SY5Y cells were transfected to overexpress CBS, these cells were able to synthesize H2S when exposed to high levels of enzyme substrates but not substrate concentrations that may reflect normal physiological conditions. At the same time, these cells demonstrated exacerbated cell death when subjected to oxygen and glucose deprivation (OGD) together with high substrate concentrations, indicating that H2S production has a detrimental effect on cell survival. This effect could be abolished by CBS inhibition. The same effect was observed with primary astrocytes exposed to OGD and high substrates or sodium hydrosulfide. In addition, CBS was upregulated and activated by truncation in primary astrocytes subjected to OGD. When rats were subjected to permanent middle cerebral artery occlusion, CBS activation was also observed. These results imply that in acute ischemic conditions, CBS is upregulated and activated by truncation causing an increased production of H2S, which exacerbate the ischemic injuries. Therefore, CBS inhibition may be a viable approach to stroke treatment.
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