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Possibly, with respect to the underlying disease (which was markedly counteracted in BPC 157 rats), more activity of eNOS (the constitutive isoforms instantly increase along with COX2), and more activity of nNOS (NO produced by nNOS is thought to mediate synaptic plasticity and neuronal signaling) [103,104], may be intrinsic effects of BPC 157
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Importantly, neuronal cell death in response to ischemic stress conditions in vitro was significantly alleviated in Phd2 deficient neurons (Figure 2G)
