| First Author | Meng C | Year | 2020 |
| Journal | Mol Med Rep | Volume | 22 |
| Issue | 5 | Pages | 4213-4220 |
| PubMed ID | 33000218 | Mgi Jnum | J:305681 |
| Mgi Id | MGI:6705251 | Doi | 10.3892/mmr.2020.11532 |
| Citation | Meng C, et al. (2020) IKKepsilon deficiency inhibits acute lung injury following renal ischemia reperfusion injury. Mol Med Rep 22(5):4213-4220 |
| abstractText | Renal ischemia reperfusion injury (IRI) after surgery may promote acute lung injury (ALI) by inducing an inflammatory response. However, the underlying molecular mechanism is still unclear. Studies have reported that inhibitor of kappaB kinase (IKK)epsilon primarily regulates inflammation and cell proliferation. The present study aimed to investigate the regulatory role of IKKepsilon in ALI in mice, in order to provide an experimental basis for preventing ALI following surgeryinduced renal IRI. C57BL/6J wildtype (WT) and IKKepsilon knockout (IKKepsilon/) mice underwent bilateral renal pedicle occlusion. The plasma creatinine concentration, urea nitrogen level and lung wettodry ratio were measured at baseline, and at 24 and 48 h after declamping. The histological localization and protein levels of inflammatory factors, such as tumor necrosis factor (TNF)alpha, interleukin (IL)1beta and IL10, were analyzed in lung tissues. Subsequently, the interactions between IKKepsilon and components of the nuclear factor (NF)kappaB pathway were studied. The results of the present study demonstrated that the IKKepsilon/ groups displayed similar renal function but less pulmonary edema compared with that of the WT groups. The levels of proinflammatory factors in the lungs were significantly upregulated in WT mice compared with those in IKKepsilon/ mice after IRI surgery. The NFkappaB pathway components and downstream factors were substantially upregulated in the WT groups after acute ischemic kidney injury, and these effects were significantly inhibited in the IKKepsilon/ groups. Based on these data, the present study hypothesized that IKKepsilon may serve a negative role in kidneylung crosstalk after renal IRI and may be a novel target for the treatment of patients with renal IRI. |
