Abstract
BackgroundExposure to paraquat results in acute lung injury. A systemic inflammatory response has been widely established as a contributor to paraquat-induced acute lung injury. Recent studies have reported that consumption of Xuebijing prevents inflammatory response-induced diseases. This study investigated whether consumption of Xuebijing protected rats against paraquat-induced acute lung injury.MethodsAdult male Sprague Dawley rats were randomly divided into four groups: control group; paraquat group; paraquat + Xuebijing group; and paraquat + dexamethasone group. Rats in the paraquat, paraquat + Xuebijing and paraquat + dexamethasone groups were intraperitoneally injected with paraquat (30 mg/kg) or administered paraquat and Xuebijing at 8 mL/kg or dexamethasone at 5 mg/kg, respectively, via an injection into the tail vein. Lung p38 MAPK, NF-κB65, IkB, p-IκB-α, HIF-1α, Nrf2 and TGF-β1 expression were essayed using western blotting. IL-6, TNF-α, IL-1β, IL-10, TGF-β1 and PIIIP were measured using ELISA. ROS, oxidised glutathione and glutathione activity were measured.ResultsAfter inducing acute lung injury with paraquat for 24 h, Xuebijing was observed to block lung p-p38 MAPK, NF-κB65, HIF-1α, p-IκB-α and TGF-β1 expression, and increased Nrf2 and IkB expression. The numbers of neutrophils and lymphocytes and total number of cells were significantly lower in the Xuebijing group compared with the control group. IL-6, TNF-α, IL-1β, TGF-β1 and PIIIP levels were significantly decreased in the Xuebijing group. ROS and oxidised glutathione activity were markedly inhibited by Xuebijing. Histological evaluation showed attenuation of the effects of Xuebijing on paraquat-induced lung injury. Compared with the paraquat + dexamethasone group, the Xuebijing + paraquat group showed no significant differences.ConclusionsInhibiting the expression of p38 MAPK and NF-κB65 was crucial for the protective effects of Xuebijing on paraquat-induced acute lung injury. The findings suggest that Xuebijing could effectively ameliorate paraquat-induced acute lung injury in rats. Xuebijing was as effective as dexamethasone at improving paraquat-induced lung injury by regulating lung inflammation, lung function and oxidative stress responses.
Highlights
Exposure to paraquat results in acute lung injury
Xuebijing + paraquat group rats displayed moderate injury, but the severity was significantly ameliorated and lung injury score significantly decreased compared with the paraquat group, and compared with the dexamethasone + paraquat group, there were no significant differences
Xuebijing inhibited the expression of p-p38 mitogen-activated protein kinase (MAPK), NF-κB65, p-IkB-α, Hypoxia-inducible factor-1α (HIF-1α) and TGF-β1, and up-regulated IkB and nuclear factor E2-related factor 2 (Nrf2) in paraquat-induced lung tissue To assess the potential role of Xuebijing in paraquatinduced acute lung injury (ALI), we determined the levels of p-p38 MAPK, NF-κB65, IkB, p-IκB-α, hypoxia-inducible factor (HIF)-1α, Nrf2 and TGF-β1 proteins in lung tissue of paraquat-induced ALI rats using western blotting at 24 h after paraquat challenge (Figure 3)
Summary
Exposure to paraquat results in acute lung injury. A systemic inflammatory response has been widely established as a contributor to paraquat-induced acute lung injury. Recent studies have reported that consumption of Xuebijing prevents inflammatory response-induced diseases. This study investigated whether consumption of Xuebijing protected rats against paraquat-induced acute lung injury. Because of its selective accumulation in the lungs, it causes severe lung injury, manifesting in oedema, haemorrhage, interstitial inflammation, and progressive fibrosis [1,2]. Many studies have suggested that the mechanisms of paraquat-induced lung injury are mainly associated with the systemic inflammatory response [3,4]. Acute lung injury (ALI) in humans is characterised by a severe acute inflammatory response in the lungs and neutrophilic alveolitis [5]. New strategies are still required to achieve effective treatment of ALI, which might aid in clinical therapy for ALI patients
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