Effects of chrysin and early exercise on NF-κB signaling pathway during lung injury induced by focal cerebral ischemia-reperfusion in rats

Abstract

Inflammation and oxidative stress play an integral role in the pathogenesis of cerebral ischemia. Chrysin exhibits anti-inflammatory and neuroprotective effects. Early exercise is an effective strategy for stroke treatment. However, the signaling pathways that link these events are not fully understood. We investigated the effects signaling pathways of chrysin treatment with early exercise in a rat model of lung injury induced by transient focal cerebral ischemia. Forty female healthy SD rats were divided into four s randomly ( n = 10): sham operation (A), lung injury induced by ischemia-reperfusion (B), chrysin treatment (C), and chrysin + early exercise (D). In C, rats were treated intragastrically with chrysin every day at a dose of 20 mg/kg while rats were treated intragastrically with the same volume of NS in A and B. In D, rats received forced treadmill training and were treated intragastrically with chrysin (20 mg/kg). Fourteen days later, all rats were sacrificed. Brain and lung tissues were obtained for pathological analysis, lung water content and lung function were assessed. Meanwhile, qRT–PCR and western blotting were employed to detect the expression of NF-κB and TNF–α in lung. Neurobehavioral deficits and lung injury could be seen in B. Compared with B, chrysin (C and D) successfully decreased the infarct size, relieved pulmonary edema and improves lung function, while downregulated expression of NF-κB and TNF–α. Notably, neurobehavioral deficits and lung injury were significantly improved in D, as well as the decreased expression of NF-κB and TNF–α. Chrysin treatment with early exercise improved functional outcomes and abrogated the lung injury induced by focal cerebral ischemia-reperfusion on rats, which might be associated with inhibition of NF-κB-mediated neuroinflammation. Chrysin combined with early exercise may be used as a potential treatment in patients at high risk of lung injury induced by ischemic stroke.