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Leptin treatment at a dose used for gene expression (i.e., 5 mg/kg, i.p.) failed to induce a change in phosphorylation levels of STAT3 or ERK ( t (7) = 0.5803, P = 0.5782), but significantly increased AKT phosphorylation ( t (7) = 3.8020, P = 0.0067), suggesting that leptin action in the hippocampus may be mediated by AKT signaling (Fig
Funding for this study was provided by the National Institutes of Health to CJW (R01 HL127564, R35 HL135824)
The science behind BPC-157 involves several interconnected mechanisms that, taken together, create a more favorable environment for tissue repair
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