Protective Effects Of Camel Milk On LPS-induced ARDS Of Rats And Its Mechanism

Objective: Acute respiratory distress syndrome (ARDS) is a common clinical lung disease characterized by dangerous complication, fast progresses, and high mortality. In recent years, a large number of clinical and basic studies have shown that inflammation, oxidative stress, MAPKs signaling pathways as well as lipid signaling molecules play a key role in the occurrence and development of ARDS. Camel milk (CM) as a kind of nutrition,play a role of adjuvant therapy in various diseases. Our preliminary research results suggested that CM could inhibit the inflammatory response and lung wet/dry weight ratio, improve the severity of the inflammation of lung tissue pathological changes to protect the ARDS rats induced by lipopolysaccharide. Based on the above research results,the present study intended to explore the effect of camel milk on oxidative stress, MAPKs signaling pathways and the role of lipid signaling molecules in lipopolysaccharides (LPS) induced ARDS rat model. This will provide a new theoretical support for clinical diagnosis and treatment of ARDS.Methods: 48 healthy adult male Wistar rats were randomly divided into four group: control group (Control group),model group (LPS group, 20 mg/Kg), treatment group (CM + LPS group, CM: 10 mL/Kg) and camel milk control group (CM). CM preconditioning in rats after 14 days, 6 h after intraperitoneal injection of lipopolysaccharide build mould execution, to detect enzyme-linked immunosorbent assay (ELISA) determination of lung tissue homogenate myeloperoxidase (MPO), malondialdehyde (MDA) and total antioxidant capacity (TAOC) activity and serum sphingosine 1-phosphate (SlP), lysophosphatide acid (LPA) content; Western blot technique to detect MAPKs signaling pathways in the key regulatory proteins (P38/p-P38, JNK/p-JNK, ERK/p-ERK) activation state.Results: Compared with model group, camel milk significantly decreased in lung tissue homogenate myeloperoxidase, malondialdehyde content, improved the activity of total antioxidant capacity, reduced serum sphingosine 1-phosphate, lysophosphatide phosphate acid content. According to the results of Western blot, camel milk pretreatment could block phosphorylation of ERK, P38 and JNK, inhibit LPS induced crack the original activated protein kinase signaling pathway, the result was statistically significant (P < 0.05). No difference between normal group and the camel milk control group, the result has no statistical significance (P > 0.05).Conclusion: Camel milk could alleviate the ARDS damage in rats induced by lipopolysaccharidearise through relieving oxidative stress, reducing lipid signaling molecules and inhibiting the activation of MAPKs pathway.