Limits...
3,5,4'-Tri-O-acetylresveratrol Attenuates Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome via MAPK/SIRT1 Pathway.

Ma L, Zhao Y, Wang R, Chen T, Li W, Nan Y, Liu X, Jin F - Mediators Inflamm. (2015)

Bottom Line: The results showed that AC-Rsv significantly reduced the mortality of mice stimulated with LPS.What was more, AC-Rsv and Rsv treatment reduced the secretion of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells, respectively.More importantly, in vivo results have also demonstrated that the protecting effects of Rsv on LPS-induced inflammation would be neutralized when SIRT1 was in-hibited by EX527.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiration, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.

ABSTRACT
The aim of the present research was to investigate the protecting effects of 3,5,4'-tri-O-acetylresveratrol (AC-Rsv) on LPS-induced acute respiratory distress syndrome (ARDS). Lung injuries have been evaluated by histological examination, wet-to-dry weight ratios, and cell count and protein content in bronchoalveolar lavage fluid. Inflammation was assessed by MPO activities and cytokine secretion in lungs and cells. The results showed that AC-Rsv significantly reduced the mortality of mice stimulated with LPS. Pretreatment of AC-Rsv attenuated LPS-induced histological changes, alleviated pulmonary edema, reduced blood vascular leakage, and inhibited the MPO activities in lungs. What was more, AC-Rsv and Rsv treatment reduced the secretion of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells, respectively. Further exploration revealed that AC-Rsv and Rsv treatment relieved LPS-induced inhibition on SIRT1 expression and restrained the activation effects of LPS on MAPKs and NF-κB activation both in vitro and in vivo. More importantly, in vivo results have also demonstrated that the protecting effects of Rsv on LPS-induced inflammation would be neutralized when SIRT1 was in-hibited by EX527. Taken together, these results indicated that AC-Rsv protected lung tissue against LPS-induced ARDS by attenuating inflammation via p38 MAPK/SIRT1 pathway.

No MeSH data available.


Related in: MedlinePlus

Effects of AC-Rsv on LPS-induced mortality in mice. Mice from each experimental group were injected with 20 mg/kg of LPS with or without pretreatment of AC-Rsv (25, 50, and 100 mg/kg) for 7 days. Alive mice in each group were counted every 12 h. The accumulative mortalities of mice in middle-dose (50 mg/kg) and high-dose (100 mg/kg) groups were 55% and 65%, respectively, which were significantly lower than that of LPS group (80% mice dead) (P < 0.05). More importantly, 50 mg/kg of AC-Rsv exhibited the best protecting effect, P < 0.05, n = 20.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4663353&req=5

fig2: Effects of AC-Rsv on LPS-induced mortality in mice. Mice from each experimental group were injected with 20 mg/kg of LPS with or without pretreatment of AC-Rsv (25, 50, and 100 mg/kg) for 7 days. Alive mice in each group were counted every 12 h. The accumulative mortalities of mice in middle-dose (50 mg/kg) and high-dose (100 mg/kg) groups were 55% and 65%, respectively, which were significantly lower than that of LPS group (80% mice dead) (P < 0.05). More importantly, 50 mg/kg of AC-Rsv exhibited the best protecting effect, P < 0.05, n = 20.

Mentions: In order to assess the protecting effects of AC-Rsv on endotoxemia, we firstly evaluated the effects of AC-Rsv on LPS-induced mortality in mice. As shown in Figure 2, the accumulative mortalities of mice in middle-dose (50 mg/kg) and high-dose (100 mg/kg) groups were 55% and 65%, respectively, which were significantly lower than that of LPS group (80% mice dead) (P < 0.05). Those data indicated that AC-Rsv protected mice from LPS-induced death and 50 mg/kg of AC-Rsv exhibited the best protecting effects which was adopted to carry out further researches.


3,5,4'-Tri-O-acetylresveratrol Attenuates Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome via MAPK/SIRT1 Pathway.

Ma L, Zhao Y, Wang R, Chen T, Li W, Nan Y, Liu X, Jin F - Mediators Inflamm. (2015)

Effects of AC-Rsv on LPS-induced mortality in mice. Mice from each experimental group were injected with 20 mg/kg of LPS with or without pretreatment of AC-Rsv (25, 50, and 100 mg/kg) for 7 days. Alive mice in each group were counted every 12 h. The accumulative mortalities of mice in middle-dose (50 mg/kg) and high-dose (100 mg/kg) groups were 55% and 65%, respectively, which were significantly lower than that of LPS group (80% mice dead) (P < 0.05). More importantly, 50 mg/kg of AC-Rsv exhibited the best protecting effect, P < 0.05, n = 20.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4663353&req=5

fig2: Effects of AC-Rsv on LPS-induced mortality in mice. Mice from each experimental group were injected with 20 mg/kg of LPS with or without pretreatment of AC-Rsv (25, 50, and 100 mg/kg) for 7 days. Alive mice in each group were counted every 12 h. The accumulative mortalities of mice in middle-dose (50 mg/kg) and high-dose (100 mg/kg) groups were 55% and 65%, respectively, which were significantly lower than that of LPS group (80% mice dead) (P < 0.05). More importantly, 50 mg/kg of AC-Rsv exhibited the best protecting effect, P < 0.05, n = 20.
Mentions: In order to assess the protecting effects of AC-Rsv on endotoxemia, we firstly evaluated the effects of AC-Rsv on LPS-induced mortality in mice. As shown in Figure 2, the accumulative mortalities of mice in middle-dose (50 mg/kg) and high-dose (100 mg/kg) groups were 55% and 65%, respectively, which were significantly lower than that of LPS group (80% mice dead) (P < 0.05). Those data indicated that AC-Rsv protected mice from LPS-induced death and 50 mg/kg of AC-Rsv exhibited the best protecting effects which was adopted to carry out further researches.

Bottom Line: The results showed that AC-Rsv significantly reduced the mortality of mice stimulated with LPS.What was more, AC-Rsv and Rsv treatment reduced the secretion of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells, respectively.More importantly, in vivo results have also demonstrated that the protecting effects of Rsv on LPS-induced inflammation would be neutralized when SIRT1 was in-hibited by EX527.

View Article: PubMed Central - PubMed

Affiliation: Department of Respiration, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China.

ABSTRACT
The aim of the present research was to investigate the protecting effects of 3,5,4'-tri-O-acetylresveratrol (AC-Rsv) on LPS-induced acute respiratory distress syndrome (ARDS). Lung injuries have been evaluated by histological examination, wet-to-dry weight ratios, and cell count and protein content in bronchoalveolar lavage fluid. Inflammation was assessed by MPO activities and cytokine secretion in lungs and cells. The results showed that AC-Rsv significantly reduced the mortality of mice stimulated with LPS. Pretreatment of AC-Rsv attenuated LPS-induced histological changes, alleviated pulmonary edema, reduced blood vascular leakage, and inhibited the MPO activities in lungs. What was more, AC-Rsv and Rsv treatment reduced the secretion of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells, respectively. Further exploration revealed that AC-Rsv and Rsv treatment relieved LPS-induced inhibition on SIRT1 expression and restrained the activation effects of LPS on MAPKs and NF-κB activation both in vitro and in vivo. More importantly, in vivo results have also demonstrated that the protecting effects of Rsv on LPS-induced inflammation would be neutralized when SIRT1 was in-hibited by EX527. Taken together, these results indicated that AC-Rsv protected lung tissue against LPS-induced ARDS by attenuating inflammation via p38 MAPK/SIRT1 pathway.

No MeSH data available.


Related in: MedlinePlus