Protective effect of astaxanthin on tuberculosis-associated inflammatory lung injury

Mycobacterium tuberculosis (MTB) invades the lungs and is the key cause of tuberculosis (TB). MTB induces immune overreaction and inflammatory damage to lung tissue. There is a lack of protective drugs against pulmonary inflammatory damage. Herein, the protective roles and mechanisms of Astaxanthin (ASTA), a natural compound, in inflammatory injured lung epithelial cells were investigated. Lipopolysaccharide (LPS) was used to establish inflammatory injury model in the murine lung epithelial (MLE)-12 cells. Cell counting kit-8 was used for screening of compound concentrations. Cell proliferation was observed real-time with a high content analysis system. Flow cytometry assessed Apoptosis. The changes of apoptotic proteins and key proteins in nuclear factor kappa-B (NF-κB) pathway were measured with the western blot. LPS was used to establish an animal model of pulmonary injury. The pathological changes and degree of inflammatory injury in lung tissue were observed with hematoxylin and eosin (HE) staining. The levels of inflammatory mediators were detected with enzyme-linked immunosorbent assay. The results showed that ASTA reduced lung inflammation and attenuated inflammatory damage in lung tissues. ASTA reduced Apoptosis stimulated by LPS through suppressing the NF-κB pathway in MLE-12 cells. We believe that ASTA may have great potential for protection against inflammatory damage to lung tissue.

Astaxanthin; NF-κB signaling pathway; Tuberculosis; apoptosis; flow cytometry; inflammatory lung injury.