The aim of this study was to investigate the effects of Astragaloside IV (AS) on cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD). Our results showed that AS alleviated CS-induced pathological injury in lung tissue. AS also increased superoxide dismutase (SOD) and reduced the level of malondialdehyde (MDA) in serum and lung. AS also reduced cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in serum and lung. More, AS significantly reduced the protein expression of JAK3/STAT3/NF-κB pathway in CS-induced mice. In vitro, cigarette smoke extract (CSE) stimulation exposed to normal human bronchial epithelial (HBE) cells. Results further confirmed that AS significantly inhibited the protein levels of JAK3/STAT3/NF-κB pathway in CSE-induced HBE. Our result showed that AS might effectively ameliorate COPD via JAK3/STAT3/NF-κB pathway.
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This work was supported by National Natural Science Project (81470225).
Conflict of Interest
The authors declare that they have no conflict of interest.
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Meiqian, Z., Leying, Z. & Chang, C. Astragaloside IV Inhibits Cigarette Smoke-Induced Pulmonary Inflammation in Mice. Inflammation 41, 1671–1680 (2018). https://doi.org/10.1007/s10753-018-0811-x
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