Acute lung injury (ALI) is a critical syndrome that is associated with a high morbidity and mortality in patients. Sevoflurane has a lung protective effect in ALI as it reportedly has anti-inflammatory and apoptotic-regulating activity. However, the mechanism is still not entirely understood. The aim of the present study was to explore the effects of sevoflurane on lipopolysaccharide (LPS)-induced ALI in mice and the possible mechanisms involved. The results revealed that sevoflurane treatment improved LPS-induced lung injury, as evidenced by the reduction in mortality, lung permeability, lung wet/dry ratio and lung histopathological changes in mice. Total cell counts and the production of pro-inflammatory cytokines [tumor necrosis factor-α, interleukin (IL)-1β and IL-6] in bronchoalveolar fluid were also decreased following treatment with sevoflurane. Additionally, LPS-triggered apoptosis in lung tissues, which was eliminated by sevoflurane. Furthermore, a miRCURY™ LNA array was employed to screen for differentially expressed microRNAs (miRs/miRNAs). Among these miRNAs, 6 were differentially expressed and were involved in the inflammatory response, but only miR-27a-3p (miR-27a) was regulated by sevoflurane. Subsequently, the present study investigated whether sevoflurane exerts its function through the modulation of miR-27a. The results demonstrated that the overexpression of miR-27a via an injection with agomiR-27a produced similar protections as sevoflurane, while the inhibition of miR-27a suppressed the lung protective effects of sevoflurane in ALI mice. In addition, the present study identified that miR-27a inhibited Toll-like receptor 4 (TLR4) by binding to its 3′-untranslated region. Western blot analysis demonstrated that sevoflurane may ameliorate the inflammatory response by blocking the miR-27a/TLR4/MyD88/NF-κB signaling pathway. The present results indicate that sevoflurane may be a viable therapeutic option in the treatment of patients with ALI.

Sevoflurane treatment can attenuate lung inflammation in rats with lipopolysaccharide-induced acute lung injury.

We studied the in vitro anti-tumor activity of Bidens Bipinnata L. extract. MTT assay was used to investigate the inhibitory effect of different concentrations of the extracts on human hepatocellular carcinoma (HepG2) cell lines and human cervical carcinoma (Hela) cell lines, and the IC 50 values were calculated. The Bidens Bipinnata L. extract had different degrees of inhibitory effects on these two cells, and when exposure time was 48 h, the inhibition rate reached its peak, with IC 50 values of 14.80 μg/mL and 13.50 μg/mL respectively. The Bidens Bipinnata L. extract had a good inhibitory effect on human HepG2 cell lines and Hela cell lines, and thus has certain development prospects.