We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
The protective effect of fidocaine on lipopolysaccharide-induced acute fung injury in rats through NF-κB and p38 MAPK signaling pathway and excessive inflammatory responses.
- Authors
CHEN, L.-J.; DING, Y.-B.; MA, P.-L.; JIANG, S.-H.; LI, K.-Z.; LI, A.-Z.; LI, M.-C.; SHI, C.-X.; DU, J.; ZHOU, H.-D.
- Abstract
OBJECTIVE: Acute lung injury is a severe disease with a high rate of mortality, leading to more important illness. We aimed at exploring the protective role and potential mechanisms of lidocaine on lipopolysaccharide (LPS)-induced acute lung injury (ALI). MATERIALS AND METHODS: Sprague Dawley (SD) rats were randomly assigned to control group receiving 0.9% saline solution, LPS group treated with 4 mg/kg LPS i.p., LPS + lidocaine (treated with 4 mg/kg LPS i.p. followed by giving 1 mg/kg, 3 mg/kg, 5 mg/kg of lidocaine i.v.). Lung specimens and the bronchoalveolar lavage fluid (BALF) were collected for histopathological examination and biochemical analyze 12 h after LPS induction. The cytokines expression of TNF-α, IL-6 and MCP-1 was measured by ELISA. In addition, the malondialdehyde (MDA) content, the activities of total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) in lung tissues were also detected using ELISA. The protein expressions of p38, p-p38, p65, p-p65 and IκB were analyzed by Western blot. RESULTS: The results indicated that after lidocaine treatment was able to decrease significantly wet-to-dry (W/D) ratio and ameliorate the histopathologic damage. Additionally, total protein content and the number of leukocytes in BALF significantly decreased. ELISA result indicated that the levels of TNF-α, IL-6 and MCP-1 in BALF were markedly suppressed. Meanwhile, the activities of T-AOC and SOD in lung tissues significantly increased, while the content of MDA significantly decreased after treatment with lidocaine. Moreover, Western blot suggested that lidocaine inhibited phosphorylation of NF-κB p65 and p38 MAPK. CONCLUSIONS: Therefore, lidocaine could ameliorate the LPS-induced lung injury via NF-κB/p38 MAPK signaling and excessive inflammatory responses, providing a potential for becoming the anti-inflammatory agent against lung injury.
- Subjects
LUNG injuries; CHEST injuries; RESPIRATORY organ injuries; INFLAMMATION; LIPOPOLYSACCHARIDES
- Publication
European Review for Medical & Pharmacological Sciences, 2018, Vol 22, Issue 7, p2099
- ISSN
1128-3602
- Publication type
Article