Salidroside Attenuates LPS-Induced Acute Lung Injury in Rats
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ORIGINAL ARTICLE
Salidroside Attenuates LPS-Induced Acute Lung Injury in Rats Liu Jingyan,1 Guo Yujuan,1 Yang Yiming,1 Zhu Lingpeng,1 Yan Tianhua,1,3 and Miao Mingxing2,3
Abstract— The purpose of the present study was to investigate the effects of salidroside (Sal) on lung injury in lipopolysaccharide (LPS)-induced endotoxemic in vitro and in vivo. SD rats were randomly divided into five groups: control group, LPS group (15 mg kg−1), LPS plus dexamethasone (2 mg kg−1), and LPS plus Sal groups with different Sal doses (20 mg kg−1, 40 mg kg−1). Wet-to-dry weight (W/D) ratio was performed. Hematoxylin–eosin (HE) staining of lung was performed. Lung level of myeloperoxidase (MPO) was measured. Serum levels of the activities of the anti-oxidant superoxide dismutase (SOD), glutathione peroxidase (GSH-px), glutathione (GSH), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were measured. Caveolin-1 and TLR/NF-κB pathway proteins were detected by Western blot. In vitro, we evaluated the protective effect of Sal on A549 cell line induced by LPS. The activities of the antioxidant SOD, CAT, GSH and GPX, TNF-α, IL6, and IL-1β in cellular supernatant were measured. Caveolin-1 and TLR/NF-κB pathway was examined by Western blot. As a result, Sal significantly attenuated the above indices. In addition, Sal exerts pronounced protective effects in rats subjected to LPS possibly through inhibiting the caveolin-1 and TLR/NF-κB pathway in vivo. Our results indicated that Sal could be a potential therapeutic agent for the treatment of lung injury disease. KEY WORDS: salidroside; LPS; lung injury; caveolin-1; TLR/NF-κB.
INTRODUCTION Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) are conditions characterized by acute severe hypoxia that is caused by onset of pulmonary inflammation due to infection, shock, trauma, and burns, as well as other non-cardiac disease [1]. Inflam1
Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, China 2 National Experimental Teaching Demonstration Center of Pharmacy, China Pharmaceutical University, Nanjing, China 3 To whom correspondence should be addressed to Yan Tianhua at Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, China. E-mail: [email protected]; and Miao Mingxing at National Experimental Teaching Demonstration Center of Pharmacy, China Pharmaceutical University, Nanjing, China. E-mail: [email protected]
mation plays a key role in the pathogenesis of ALI [2]. Direct or indirect injury to the lung such as pneumonia, trauma, or sepsis, can cause lung inflammation [3, 4]. Caveolae were first discovered in the 1950s and observed as small, 50–100 nm, cave-like invaginations in the plasma membrane. Caveolins require certain structural components for formation: caveolin-1 (Cav-1), caveolin2, and caveolin-3. Each of these coat proteins have specific roles which can vary from cell type to cell type [5, 6]. Cav1 has been associated with a number of biological
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