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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 the expression of MAPK/SIRT1 axis in lungs were evaluated by western blot. Relative expression levels of p-p38 MAPK, p-ERK, and p-NF-κB were normalized to the expression levels of their total forms; SIRT1 expression was expressed by comparing with that of β-actin. Administration of LPS significantly decreased the SIRT1 expression and increased the expression of p-p38 MAPK, p-ERK, and p-NF-κB in lungs compared with that of control, ∗P < 0.05 versus control, while AC-Rsv treatment dramatically decreased expression of p-p38 MAPK, p-ERK, and p-NF-κB and enhanced the SIRT1 expression in lungs when challenged by LPS. ∗∗P < 0.05 versus ∗P.
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fig6: Effects of AC-Rsv on the expression of MAPK/SIRT1 axis in lungs were evaluated by western blot. Relative expression levels of p-p38 MAPK, p-ERK, and p-NF-κB were normalized to the expression levels of their total forms; SIRT1 expression was expressed by comparing with that of β-actin. Administration of LPS significantly decreased the SIRT1 expression and increased the expression of p-p38 MAPK, p-ERK, and p-NF-κB in lungs compared with that of control, ∗P < 0.05 versus control, while AC-Rsv treatment dramatically decreased expression of p-p38 MAPK, p-ERK, and p-NF-κB and enhanced the SIRT1 expression in lungs when challenged by LPS. ∗∗P < 0.05 versus ∗P.

Mentions: In order to further illustrate the mechanisms of how AC-Rsv exhibited the protecting effects against the endotoxemia induced by LPS, the expression of MAPK/SIRT1 pathway was evaluated by western blot. The results (Figure 6) showed that administration of LPS significantly decreased the SIRT1 expression and increased the expression of p-p38 MAPK, p-ERK, and p-NF-κB (P < 0.05). However, pretreatment of AC-Rsv dramatically decreased p-p38 MAPK, p-ERK, and p-NF-κB expression and enhanced the expression of SIRT1 in lungs stimulated with LPS (P < 0.05).


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 the expression of MAPK/SIRT1 axis in lungs were evaluated by western blot. Relative expression levels of p-p38 MAPK, p-ERK, and p-NF-κB were normalized to the expression levels of their total forms; SIRT1 expression was expressed by comparing with that of β-actin. Administration of LPS significantly decreased the SIRT1 expression and increased the expression of p-p38 MAPK, p-ERK, and p-NF-κB in lungs compared with that of control, ∗P < 0.05 versus control, while AC-Rsv treatment dramatically decreased expression of p-p38 MAPK, p-ERK, and p-NF-κB and enhanced the SIRT1 expression in lungs when challenged by LPS. ∗∗P < 0.05 versus ∗P.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig6: Effects of AC-Rsv on the expression of MAPK/SIRT1 axis in lungs were evaluated by western blot. Relative expression levels of p-p38 MAPK, p-ERK, and p-NF-κB were normalized to the expression levels of their total forms; SIRT1 expression was expressed by comparing with that of β-actin. Administration of LPS significantly decreased the SIRT1 expression and increased the expression of p-p38 MAPK, p-ERK, and p-NF-κB in lungs compared with that of control, ∗P < 0.05 versus control, while AC-Rsv treatment dramatically decreased expression of p-p38 MAPK, p-ERK, and p-NF-κB and enhanced the SIRT1 expression in lungs when challenged by LPS. ∗∗P < 0.05 versus ∗P.
Mentions: In order to further illustrate the mechanisms of how AC-Rsv exhibited the protecting effects against the endotoxemia induced by LPS, the expression of MAPK/SIRT1 pathway was evaluated by western blot. The results (Figure 6) showed that administration of LPS significantly decreased the SIRT1 expression and increased the expression of p-p38 MAPK, p-ERK, and p-NF-κB (P < 0.05). However, pretreatment of AC-Rsv dramatically decreased p-p38 MAPK, p-ERK, and p-NF-κB expression and enhanced the expression of SIRT1 in lungs stimulated with LPS (P < 0.05).

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