The dynamic detection of NO during the ischemic postconditioning against global cerebral ischemia/reperfusion injury

Nitric Oxide ◽  
2014 ◽  
Vol 38 ◽  
pp. 17-25 ◽  
Author(s):  
Kezhou Liu ◽  
Ming Yan ◽  
Xiaoxiang Zheng ◽  
Yong Yang
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
Global Cerebral Ischemia ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Dynamic Detection

scholarly journals A Novel Neuroprotective Strategy for Ischemic Stroke: Transient Mild Acidosis Treatment by CO2 Inhalation at Reperfusion

2013 ◽  
Vol 34 (2) ◽  
pp. 275-283 ◽  
Author(s):  
Yan-Ying Fan ◽  
Zhe Shen ◽  
Ping He ◽  
Lei Jiang ◽  
Wei-wei Hou ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
Cerebral Ischemia Reperfusion ◽  
Mptp Opening ◽  
Neuroprotective Strategy ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Cerebral Arterial Occlusion

Acidosis is one of the key components in cerebral ischemic postconditioning that has emerged recently as an endogenous strategy for neuroprotection. We set out to test whether acidosis treatment at reperfusion can protect against cerebral ischemia/reperfusion injury. Adult male C57BL/6 J mice were subjected to 60-minute middle cerebral arterial occlusion followed by 24-hour reperfusion. Acidosis treatment by inhaling 10%, 20%, or 30% CO2 for 5 or 10 minutes at 5, 50, or 100 minutes after reperfusion was applied. Our results showed that inhaling 20% CO2 for 5 minutes at 5 minutes after reperfusion-induced optimal neuroprotection, as revealed by reduced infarct volume. Attenuating brain acidosis with NaHCO3 significantly compromised the acidosis or ischemic postconditioning-induced neuroprotection. Consistently, both acidosis-treated primary cultured cortical neurons and acute corticostriatal slices were more resistant to oxygen–glucose deprivation/reperfusion insult. In addition, acidosis inhibited ischemia/reperfusion-induced apoptosis, caspase-3 expression, cytochrome c release to cytoplasm, and mitochondrial permeability transition pore (mPTP) opening. The neuroprotection of acidosis was inhibited by the mPTP opener atractyloside both in vivo and in vitro. Taken together, these findings indicate that transient mild acidosis treatment at reperfusion protects against cerebral ischemia/reperfusion injury. This neuroprotection is likely achieved, at least partly, by inhibiting mPTP opening and mitochondria-dependent apoptosis.

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