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...
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.
Quinolinic acid (QUIN) excitotoxicity is mediated by elevated intracellular
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....
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...
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.
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
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.
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
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.