Saturated hydrogen saline attenuates endotoxin-induced acute liver dysfunction in rats

Title:

Saturated hydrogen saline attenuates endotoxin-induced acute liver dysfunction in rats

Creator:

Xu, X.-F. and Zhang, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:3cf56750-e07f-4a1c-a5d5-34e8b2e63b9a
uuid:3cf56750-e07f-4a1c-a5d5-34e8b2e63b9a

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, saturated hydrogen saline, acute liver dysfunction, LPS, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

To determine the effect of saturated hydrogen saline on lipopolysaccharide (LPS)-induced acute liver dysfunction, rats were divided into control, LPS, and LPS plus saturated hydrogen saline (LPS+H 2 ) groups. Treatment with saturated hydrogen saline prolonged the median su rvival time and reduced liver dysfunction. Moreover, saturated hydrogen saline significantly reduced pathological alterations in liver tissues, the number of ballooned hepatocytes, serum tumor necrosis factor (TNF)- α and interleukin (IL)-6 levels, and myeloperoxidase (MPO) and malondialdehyde (MDA) levels in liver tissues (P<0.05). Cell apoptosis was detected in liver tissues after LPS treatment, and attenuated by saturated hydrogen saline treatment. Saturated hydrogen saline also decreased phosphorylated extracellular signal-regulated kinase (p-ERK), phosphorylated Jun kinase (p-JNK), nuclear factor-kappa B (NF- κ B), and second mitochondria-derived activator of caspase (Smac) levels, and increased p38 activation (P<0.05). Thus, saturated hydrogen saline may attenuate LPS-induced acute liver dysfunction in rats, possibly by reducing inflammation and cell apoptosis. Mitogen- activated protein kinase (MAPK), NF- κ B, and Smac may contribute to saturated hydrogen saline-mediated liver protection., X.-F. Xu, J. Zhang., and Obsahuje seznam literatury

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2013 Volume:62 | Number:4

Harvested from:

CDK

Metadata only:

false