Neuroprotective effect

Xem 1-9 trên 9 kết quả Neuroprotective effect
  • Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Neuroprotective effects of ginsenosides Rh1 and Rg2 on neuronal cells...

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  • As the rupture most commonly occurs in “mid-aged” persons (in the most creative and productive part of life), the highest effort should be put in enabling patients to return to previous activities as soon as possible. There is universal agreement that functional treatment is the most effective way in this regardless of the used conservative or operative (open or percutaneous) method.

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  • Quinolinic acid (QUIN) excitotoxicity is mediated by elevated intracellular Ca 2+ levels, and nitric oxide-mediated oxidative stress, resulting in DNA damage, poly(ADP-ribose) polymerase (PARP) activation, NAD + deple-tion and cell death. We evaluated the effect of a series of polyphenolic compounds [i.e. epigallocatechin gallate (EPCG), catechin hydrate, curcu-min, apigenin, naringenin and gallotannin] with antioxidant properties on QUIN-induced excitotoxicity on primary cultures of human neurons....

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  • Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Neuroprotective and anti-oxidant effects of caffeic acid isolated from Erigeron annuus leaf...

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  • Because clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain’s own endogenous strategies for neuroprotection. Two endogenous mechanisms have been characterized so far, namely ischemic preconditioning and ische-mic postconditioning.

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  • In the last part of the 20th century scientists discovered drugs that made the brain more resistant to ischemia, to such an extent that cerebral tissue treated with them was only little damaged, or was not damaged at all, by an ischemic insult that badly damaged control, untreated tissue. It was the beginning of a very exciting era in neuroscience research, a period when academic and industrial scientists all pursued the research of a “neuroprotectant” that could defend the ischemic brain from irreversible damage.

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  • Second, it should not be forgot that several neuroprotectant have failed not because they lacked efficacy, but because they revealed unexpected side effects. Many NMDAreceptor antagonists were discarded because in clinical trials they showed psychedelic unwanted effects. Tirilazad, an antioxidant belonging to the “lazaroid” class of antioxidants, unexpectedly worsened outcome of ischemic stroke, a fact very likely explained by some unexpected toxic action(s) that offset its neuroprotective ability.

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  • And in fact, that neuroprotection is indeed possible is demonstrated beyond doubt by the neglected survivor of that host of neuroprotectant agents: hypothermia. Hypothermia was demonstrated to be effective in a score of animal experiments, and it has now become recommended intervention in out-of-hospital cardiac arrest. Hypothermia is not a drug, but it demonstrates that neuroprotection is a reality, not a myth. Besides, it obviously shows that animal experiments were right, humans treated with hypothermia fare better than untreated ones, just like animal studies had predicted.

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  • Pathophysiologic responses in brain after stroke are highly complex. Thus far, a singular focus on saving neurons alone has not revealed any clinically effective neuroprotectants. To address this limitation, the concept of a neu-rovascular unit was developed. Within this conceptual framework, brain function and dysfunction are manifested at the level of cell–cell signaling between neuronal, glial and vascular elements.

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