Xuerui Yan1, Lin Wu2, Bin Li3, Xianjun Meng3, Hanping Dai4, Yanan Zheng5, Junfan Fu6. 1. Berry Research Laboratory, Plant Protection College, Shenyang Agricultural University, Shenyang, People's Republic of China. 2. Jilin Province Pulan High-Tech Co., Ltd, Changchun, People's Republic of China. 3. Department of Food Sciences, Food College, Shenyang Agricultural University, Shenyang, People's Republic of China. 4. Department of Fruit Trees, Horticulture College, Shenyang Agricultural University, Shenyang, People's Republic of China. 5. Department of Forest Conservation, College of Forestry, Shenyang Agricultural University, Shenyang, People's Republic of China. 6. Berry Research Laboratory, Plant Protection College, Shenyang Agricultural University, Shenyang, People's Republic of China. Electronic address: zbyxr@126.com.
Abstract
BACKGROUND: Sepsis is a complex syndrome with high mortality, which often induces acute lung injury (ALI) and acute respiratory distress syndrome. Cyanidin-3-O-glucoside (C3G), the most active anthocyanin in the blueberry extracts, has been demonstrated to have pulmonary protective effects in some ALI models. This study aims to evaluate the potential protective effect of C3G on sepsis-evoked ALI in rats. MATERIALS AND METHODS: Cecal ligation and puncture (CLP) was performed on Sprague-Dawley rats to establish sepsis-induced ALI model. Rats were injected intraperitoneally with 10 or 30 mg/kg of C3G after CLP and then the survival was recorded every 12 h for 96 h. The pulmonary protective effects of C3G on CLP-induced ALI were evaluated at 24 h after CLP. RESULTS: The results demonstrated that C3G treatment significantly improved the survival rate of CLP rats and attenuated CLP-induced lung injury, including reduction of lung wet/dry weight ratio, protein leak, infiltration of leukocytes, and myeloperoxidase activity. In addition, C3G markedly decreased malondialdehyde content and increased superoxide dismutase activity and glutathione level. Serum levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 were also decreased by C3G administration, as well as protein expression of cyclooxygenase-2 and production of prostaglandin E2 in the lung. Furthermore, C3G treatment upregulated protein expression of inhibitors of NF-κBα and downregulated expressions of nuclear factor kappa-B (NF-κB) p65 and p-p65 in the lung, thereby inhibiting the NF-κB-DNA binding activity. CONCLUSIONS: These findings indicate that C3G exerts pulmonary protective effects on CLP-induced ALI rats. The effect may be associated with NF-κB signaling pathway suppression.
BACKGROUND: Sepsis is a complex syndrome with high mortality, which often induces acute lung injury (ALI) and acute respiratory distress syndrome. Cyanidin-3-O-glucoside (C3G), the most active anthocyanin in the blueberry extracts, has been demonstrated to have pulmonary protective effects in some ALI models. This study aims to evaluate the potential protective effect of C3G on sepsis-evoked ALI in rats. MATERIALS AND METHODS: Cecal ligation and puncture (CLP) was performed on Sprague-Dawley rats to establish sepsis-induced ALI model. Rats were injected intraperitoneally with 10 or 30 mg/kg of C3G after CLP and then the survival was recorded every 12 h for 96 h. The pulmonary protective effects of C3G on CLP-induced ALI were evaluated at 24 h after CLP. RESULTS: The results demonstrated that C3G treatment significantly improved the survival rate of CLPrats and attenuated CLP-induced lung injury, including reduction of lung wet/dry weight ratio, protein leak, infiltration of leukocytes, and myeloperoxidase activity. In addition, C3G markedly decreased malondialdehyde content and increased superoxide dismutase activity and glutathione level. Serum levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 were also decreased by C3G administration, as well as protein expression of cyclooxygenase-2 and production of prostaglandin E2 in the lung. Furthermore, C3G treatment upregulated protein expression of inhibitors of NF-κBα and downregulated expressions of nuclear factor kappa-B (NF-κB) p65 and p-p65 in the lung, thereby inhibiting the NF-κB-DNA binding activity. CONCLUSIONS: These findings indicate that C3G exerts pulmonary protective effects on CLP-induced ALI rats. The effect may be associated with NF-κB signaling pathway suppression.