CaMKK2 reduces pulmonary ischemia-reperfusion injury by regulating the AMPK pathway
Objective To investigate whether CaMKK2 alleviates lung ischemia reperfusion injury(LIRI)by regulating the AMPK pathway.Methods Forty-five 8-week-old healthy male C57BL/6 mice were evenly divided into sham group(Sham),lung ischemia-reperfusion group(IR group),and IR+CaMKK2 inhibitor group(CaMKK2 inhibitor group),15 per group.A mouse model of lung ischemia-reperfusion injury(LIRI)was established,and survival rate was evaluated by survival analysis,blood gas analysis was used to evaluate mouse respiratory function,lung wet dry weight ratio was used to evaluate pulmonary edema,HE staining was used to evaluate lung tissue pathology,and Western blot was used to analyze the expressions of NF-κ B,TNF-α and CaMKK2/AMPK/mTOR signaling pathway protein in lung tissue.Results Inhibition of CaMKK2 could increase mouse mortality caused by LIRI,exacerbate pulmonary edema and respiratory dysfunction(P＜0.05),increase infiltration of inflammatory cells in lung tissue,and increase the expression of NF-κB and TNF-α in lung tissue,exacerbate the decrease in phosphorylated AMPK and the increase in phosphorylated mTOR(P＜0.05).Conclusion The CaMKK2/AMPK/mTOR signaling pathway is involved in regulating the inflammatory response of LIRI.
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