https://www.selleckchem.com/products/sc79.html
Administration of nor-BNI or MK-801 reversed these neuroprotective effects of intranasal Dynorphin A(1-8). In summary, Dynorphin A(1-8), with advantages of intranasal administration, could be effectively delivered to central nervous system(CNS). Dynorphin A(1-8) inhibited oxidative stress and apoptosis against cerebral ischemia/reperfusion injury, affording neuroprotection through NMDA receptor and κ-opioid receptor channels. Fatigue, caused by dyspnea associated with progression of interstitial pneumonia (IP), can negatively affect patien
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