Autophagy Activation and Inflammatory Factor Inhibition: The Role of Moxibustion at CV8 in Preventing Lung Injury in Rats

Lung injury caused by sports not only affects athletes’ competitive careers but also may even cause permanent respiratory diseases that become lifelong health problems. Recent studies have shown that the pathogenesis of lung injury caused by exercise is related to changes in airway inflammatory mediators induced during exercise. Inflammation and abnormal autophagy play important roles in altering inflammatory mediator expression. In clinical practice, we found that moxibustion at CV8 can promote fatigue recovery and reduce the frequency of exercise-induced asthma attacks. To further explore the mechanism of action, we carried out an experiment. Long-term fatigue exercise can lead to decreased pulmonary function, alveolar wall thinning, and enlargement and rupture of some alveolar cavities; severe ultrastructural damage; severe mitochondrial swelling; increased serum inflammatory factors such as IL-1β, IL-18, IFN-γ, and TNF-α; increased Beclin1, NLRP3, Caspase-1, IL-1β and IL-18; and decreased p62 expression. Moxibustion at CV8 can effectively prevent long-term exercise fatigue-induced lung injury, possibly by activating autophagy to inhibit the expression of inflammatory factors and promote the balance of proinflammatory/anti-inflammatory factors.