Cocculus hirsutus ameliorates gastric and lung injuries by suppressing Src/Syk

Chen, Hongxi; Hong, Yo Han; Woo, Byoung Young; Hong, Yong Deog; Manilack, Philaxay; Souladeth, Phetlasy; Jung, Jae Hee; Lee, Woo Shin; Jeon, Mijin; Kim, Taewoo; Hossain, Mohammad Amjad; Yum, Jinwhoa; Kim, Jong-Hoon; Cho, Jae Youl

doi:10.1016/j.phymed.2021.153778

Cited by 2 publications

(1 citation statement)

References 43 publications

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“…Inhibition of Src kinase may compromise the bactericidal capacity of neutrophils, but in LPS-induced ALI, the inhibition of Src kinase and NET formation may attenuated lung injury. Similar effect of Src blockade or NET inhibition in acute lung injury has also been reported by others [ 22 , 62 ].…”

Section: Discussionsupporting

confidence: 87%

Salvianolic Acid A Protects against Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting Neutrophil NETosis

Liu

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Salvianolic acid A (SAA) is one of bioactive polyphenol extracted from a Salvia miltiorrhiza (Danshen), which was widely used to treat cardiovascular disease in traditional Chinese medicine. SAA has been reported to be protective in cardiovascular disease and ischemia injury, with anti-inflammatory and antioxidative effect, but its role in acute lung injury (ALI) is still unknown. In this study, we sought to investigate the therapeutic effects of SAA in a murine model of lipopolysaccharide- (LPS-) induced ALI. The optimal dose of SAA was determined by comparing the attenuation of lung injury score after administration of SAA at three different doses (low, 5 mg/kg; medium, 10 mg/kg; and, high 15 mg/kg). Dexamethasone (DEX) was used as a positive control for SAA. Here, we showed that the therapeutic effect of SAA (10 mg/kg) against LPS-induced pathologic injury in the lungs was comparable to DEX. SAA and DEX attenuated the increased W/D ratio and the protein level, counts of total cells and neutrophils, and cytokine levels in the BALF of ALI mice similarly. The oxidative stress was also relieved by SAA and DEX according to the superoxide dismutase and malondialdehyde. NET level in the lungs was elevated in the injured lung while SAA and DEX reduced it significantly. LPS induced phosphorylation of Src, Raf, MEK, and ERK in the lungs, which was inhibited by SAA and DEX. NET level and phosphorylation level of Src/Raf/MEK/ERK pathway in the neutrophils from acute respiratory distress syndrome (ARDS) patients were also inhibited by SAA and DEX in vitro, but the YEEI peptide reversed the protective effect of SAA completely. The inhibition of NET release by SAA was also reversed by YEEI peptide in LPS-challenged neutrophils from healthy volunteers. Our data demonstrated that SAA ameliorated ALI via attenuating inflammation, oxidative stress, and neutrophil NETosis. The mechanism of such protective effect might involve the inhibition of Src activation.

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Section: Discussionsupporting

confidence: 87%