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The present study investigated the anti-oxidative and hepatoprotective effects of Glossogyne tenuifolia (GT) Cassini, against acetaminophen-induced acute liver injury in BALB/c mice. The extracts of GT by various solvents (hot water, 50% ethanol and 95% ethanol) were compared for their 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity, reducing power, total phenolic content, and total anti-oxidant capacity. The results showed that hot water (HW) extracts of GT contained high levels of phenolics and exerted an excellent anti-oxidative capacity; thus, these were used in the animal experiment. The male BALB/c mice were randomly divided into control group, acetaminophen (APAP) group, positive control group and two GT groups at low (GT-L) and high (GT-H) dosages. The results showed that mice treated with GT had significantly decreased serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). GT-H increased glutathione levels and the ratios of reduced glutathione and oxidized glutathione (GSH/GSSG) in the liver, and inhibited serum and lipid peroxidation. This experiment was the first to determine phenolic compounds, chlorogenic acid and luteolin-7-glucoside in HW extract of GT. In conclusion, HW extract of GT may have potential anti-oxidant capacity and show hepatoprotective capacities in APAP-induced liver damaged mice. [ABSTRACT FROM AUTHOR]

Despite mechanical ventilation being a very important life-saving intervention, ventilator-induced lung injury (VILI) is related with inflammatory effects and causes high mortality. Our previous study demonstrated that the interleukin-33 (IL-33) cytokine pathway is a biomarker of VILI. The purpose of this study was to further explore the effects of hydrocortisone sodium succinate (HC) on pro-inflammatory IL-33 activation by VILI. The rats were intubated and received ventilation at 20 cmH₂O of inspiratory pressure (PC20) by a G5 ventilator for 4 h as a control group, and an intervention group received the same inspiratory pressure as well as treated with HC at 1 mg/kg at the third hour of ventilation (PC20+HC). The hemodynamic and respiratory data showed similar changes in the two groups that were exposed to VILI. The pathophysiological results showed that the HC treatment attenuated the VILI severity. Treatment of HC increased IL-33 expression in the bronchoalveolar lavage fluid (BALF). These results demonstrated that IL-33 is involved in VILI processing and HC treatment attenuated IL-33 involvement in inflammatory activation in VILI. In conclusion, IL-33 may play an important role in VILI.