Publication date: April 2017
Source:International Immunopharmacology, Volume 45
Author(s): XinGang Lu, YingXiu Pu, WeiGuang Kong, XiaoDan Tang, JiAn Zhou, HaiXin Gou, Xiao Song, HaiFeng Zhou, NingZhou Gao, Jie Shen
Acute lung injury, characterized by inflammation, is a main cause of respiratory failure that affects patients worldwide. Antidesmone is one compound mainly isolated from Ajugade cumbens Thunb (Labiatae), an herb agent of Labiatae family. In this research, we investigated the anti-inflammation effect of antidesmone in vitro and in vivo. Antidesmone exerted none apparently cytotoxicity in vitro and toxic in vivo. In vitro results demonstrated that antidesmone suppressed the excess inflammatory cytokines production, including tumor necrosis factor-α, interleukin-6 and interleukin-1β in lipopolysaccharide (LPS)-exposed RAW264.7 cells. In vivo results suggested that antidesmone inhibited inflammatory cytokines in the bronchoalveolar lavage fluid and lung tissue after LPS stimulation. Moreover, antidesmone attenuated the nuclear translocation of p65. Mechanism study revealed that mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways play important roles in antidesmone's action. Taken together, our data uncover a relative toxic anti-inflammatory drug, antidesmone, can inhibit inflammation on stimulated macrophages and thereby prevents acute lung injury by regulating MAPK and NF-κB signaling pathways.
http://ift.tt/2kcne5G
Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00302841026182,00306932607174,alsfakia@gmail.com,
Ετικέτες
Τρίτη 31 Ιανουαρίου 2017
Antidesmone, a unique tetrahydroquinoline alkaloid, prevents acute lung injury via regulating MAPK and NF-κB activities
Εγγραφή σε:
Σχόλια ανάρτησης (Atom)
-
Publication date: September 2017 Source: European Journal of Surgical Oncology (EJSO), Volume 43, Issue 9 http://ift.tt/2gezJ2D
-
Publication date: January–February 2018 Source: Materials Today, Volume 21, Issue 1 Author(s): David Bradley http://ift.tt/2BP...
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου