Research from China Pharmaceutical University Reveals New Findings on Transient Ischemic Attack [(S)-ZJM-289 preconditioning induces a late phase protection against nervous injury induced by transient cerebral ischemia and oxygen-glucose ...]
By a News Reporter-Staff News Editor at Health & Medicine Week -- A new study on Cardiovascular Diseases and Conditions is now available. According to news reporting from Nanjing, People's Republic of China, by NewsRx journalists, research stated, "(S)-ZJM-289, a novel nitric oxide (NO)-releasing derivative of 3-n-butylphthalide, induces the neuroprotection in a rat model of focal cerebral ischemia/reperfusion (I/R). However, much is unknown about the late phase effect in the neuroprotection of (S)-ZJM-289 preconditioning."
The news correspondents obtained a quote from the research from China Pharmaceutical University, "The purpose of this study is to explore the late phase neuroprotection of (S)-ZJM-289 preconditioning, as well as underlying mechanisms involved. Preconditioning with 40-160 mg/kg, (S)-ZJM-289 significantly reduces brain damage after I/R. (S)-ZJM-289 preconditioning is effective when applied 1-3 days before I/R. Moreover, the degrees of neuroprotection offered by (S)-ZJM-289 preconditioning and ischemic preconditioning are virtually identical. (S)-ZJM-289 preconditioning also protects primary cultured cortical neurons against oxygen-glucose deprivation and recovery-induced cytotoxicity in vitro. (S)-ZJM-289 preconditioning significantly increases the generation of NO, but has no effect on the nitric oxide synthase activities. Additionally, (S)-ZJM-289 preconditioning promotes the dissociation between nuclear-factor-E2-related factor (Nrf2) and kelch-like ECH-associated protein 1, and induces Nrf2 nuclear localization. The neuroprotection of (S)-ZJM-289 preconditioning is blocked by Nrf2-siRNA in vitro. (S)-ZJM-289 preconditioning up-regulates antioxidant enzymes against nervous injury. (S)-ZJM-289 preconditioning significantly activates extracellular regulated protein kinases (ERK) and inhibits c-Jun N-terminal kinases signaling cascade. The neuroprotection is abolished by the ERK inhibitor PD98059 in vitro. Subsequently, (S)-ZJM-289 preconditioning increases the levels of anti-apoptotic protein B cell lymphoma 2 (Bcl-2) and inhibited the translocation of Bcl-2 associated X to the mitochondria, thus attenuating the release of cytochrome c from the mitochondria and the activation of downstream caspase."
According to the news reporters, the research concluded: "These results suggest that (S)-ZJM-289 preconditioning exerts the late phase protection against nervous injury induced by transient cerebral ischemia and oxygen-glucose deprivation."
For more information on this research see: (S)-ZJM-289 preconditioning induces a late phase protection against nervous injury induced by transient cerebral ischemia and oxygen-glucose deprivation. Neurotoxicity Research, 2014;26(1):16-31. (Springer - www.springer.com; Neurotoxicity Research - www.springerlink.com/content/1029-8428/)
Our news journalists report that additional information may be obtained by contacting C. Zhang, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, People's Republic of China. Additional authors for this research include Z. Zhang, Q. Zhao, X. Wang, H. Ji and Y. Zhang (see also Cardiovascular Diseases and Conditions).
Keywords for this news article include: Asia, Nanjing, Chemicals, Chemistry, Chalcogens, Nitric Oxide, Brain Ischemia, Transient Ischemic Attack, People's Republic of China, Cardiovascular Diseases and Conditions.
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