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 content of cytokines in LPS stimulated lungs and NR8383 cells have been measured by ELISA. (a–c) TNF-α, IL-6, and IL-1β levels in lungs, (d–f) TNF-α, IL-6, and IL-1β levels in NR8383 cells. Data are expressed as mean ± S.D. n = 8. LPS stimulation increased the content of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells compared with that of control, ∗P < 0.05 versus control, while AC-Rsv and Rsv treatment significantly inhibited the formation of those cytokines in lung and NR8383 cells, respectively. ∗∗P < 0.05 versus ∗P.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4663353&req=5

fig5: Effects of AC-Rsv on content of cytokines in LPS stimulated lungs and NR8383 cells have been measured by ELISA. (a–c) TNF-α, IL-6, and IL-1β levels in lungs, (d–f) TNF-α, IL-6, and IL-1β levels in NR8383 cells. Data are expressed as mean ± S.D. n = 8. LPS stimulation increased the content of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells compared with that of control, ∗P < 0.05 versus control, while AC-Rsv and Rsv treatment significantly inhibited the formation of those cytokines in lung and NR8383 cells, respectively. ∗∗P < 0.05 versus ∗P.

Mentions: In order to evaluate the effects of AC-Rsv on LPS-induced inflammation in lungs, MPO activity (Figure 4) and contents of TNF-α, IL-6, and IL-1β (Figures 5(a)–5(c)) have been measured. The results revealed that LPS injection significantly upregulated the activity of MPO and increased the contents of TNF-α, IL-6, and IL-1β in lungs compared with those of control (P < 0.05). However, pretreatment of AC-Rsv dramatically decreased MPO activity and inhibited the concentration of TNF-α, IL-6, and IL-1β in lungs (P < 0.05). Also, the results indicated that AC-Rsv treatment alone did not affect the MPO activity and content of cytokines in lungs.


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 content of cytokines in LPS stimulated lungs and NR8383 cells have been measured by ELISA. (a–c) TNF-α, IL-6, and IL-1β levels in lungs, (d–f) TNF-α, IL-6, and IL-1β levels in NR8383 cells. Data are expressed as mean ± S.D. n = 8. LPS stimulation increased the content of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells compared with that of control, ∗P < 0.05 versus control, while AC-Rsv and Rsv treatment significantly inhibited the formation of those cytokines in lung and NR8383 cells, respectively. ∗∗P < 0.05 versus ∗P.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: Effects of AC-Rsv on content of cytokines in LPS stimulated lungs and NR8383 cells have been measured by ELISA. (a–c) TNF-α, IL-6, and IL-1β levels in lungs, (d–f) TNF-α, IL-6, and IL-1β levels in NR8383 cells. Data are expressed as mean ± S.D. n = 8. LPS stimulation increased the content of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells compared with that of control, ∗P < 0.05 versus control, while AC-Rsv and Rsv treatment significantly inhibited the formation of those cytokines in lung and NR8383 cells, respectively. ∗∗P < 0.05 versus ∗P.
Mentions: In order to evaluate the effects of AC-Rsv on LPS-induced inflammation in lungs, MPO activity (Figure 4) and contents of TNF-α, IL-6, and IL-1β (Figures 5(a)–5(c)) have been measured. The results revealed that LPS injection significantly upregulated the activity of MPO and increased the contents of TNF-α, IL-6, and IL-1β in lungs compared with those of control (P < 0.05). However, pretreatment of AC-Rsv dramatically decreased MPO activity and inhibited the concentration of TNF-α, IL-6, and IL-1β in lungs (P < 0.05). Also, the results indicated that AC-Rsv treatment alone did not affect the MPO activity and content of cytokines in lungs.

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