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Glutathione Supplementation Attenuates Oxidative Stress and Improves Vascular Hyporesponsiveness in Experimental Obstructive Jaundice.

Chen J, Wu F, Long Y, Yu W - Oxid Med Cell Longev (2015)

Bottom Line: We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model.The proinflammatory cytokines levels (TNF-α and IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well.All of those were reduced by the treatment of GSH.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesia & Intensive Care, Eastern Hepatobiliary Surgery Hospital, the Second Military Medical University, Shanghai 200438, China ; Department of Anesthesiology, 81st Hospital of the Chinese PLA, Nanjing 210002, China.

ABSTRACT
We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: a NS group, a GSH group, a BDL + NS group, and a BDL + GSH group. GSH was administrated into rats in the GSH and BDL + GSH groups by gastric gavage. An equal volume of normal saline was, respectively, given in the NS group and BDL + NS group. Blood was gathered for serological determination and thoracic aorta rings were isolated for measurement of isometric tension. Obstructive jaundice led to a significant increase in the serum total bilirubin, AST, and ALT levels. The proinflammatory cytokines levels (TNF-α and IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well. All of those were reduced by the treatment of GSH. Meanwhile, contraction of aorta rings to NA and vasorelaxation to ACh or SNP in the BDL group rats were markedly decreased, while GSH administration reversed this change. Our findings suggested that GSH supplementation attenuated overexpressed ONOO(-) from the reaction of excessive NO with O2 (∙-) and protected against obstructive jaundice-induced vascular hyporesponsiveness in rats.

No MeSH data available.


Related in: MedlinePlus

Response elicited by NA in rat thoracic aortic rings from NS group, GSH group, BDL + NS group, and BDL + GSH group (n = 6). Data are presented as mean ± SD. aP < 0.01 versus NS group for % maximum response; bP < 0.01 versus BDL + NS group.
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fig2: Response elicited by NA in rat thoracic aortic rings from NS group, GSH group, BDL + NS group, and BDL + GSH group (n = 6). Data are presented as mean ± SD. aP < 0.01 versus NS group for % maximum response; bP < 0.01 versus BDL + NS group.

Mentions: Cumulative addition of NA (10−9–10−5 mol/L) resulted in concentration dependent contractions in aortas of all groups. The maximum contractile responses to NA (10−8–10−5 mol/L) in the aortas from the NS group rats in the presence of endothelium were significantly (P < 0.01) greater than the BDL + NS group rats. Compared with the BDL + NS group, GSH pretreatment (BDL + GSH group) enhanced contractile response of thoracic aortic rings to NA (3 × 10−8–10−5 mol/L) (Figure 2).


Glutathione Supplementation Attenuates Oxidative Stress and Improves Vascular Hyporesponsiveness in Experimental Obstructive Jaundice.

Chen J, Wu F, Long Y, Yu W - Oxid Med Cell Longev (2015)

Response elicited by NA in rat thoracic aortic rings from NS group, GSH group, BDL + NS group, and BDL + GSH group (n = 6). Data are presented as mean ± SD. aP < 0.01 versus NS group for % maximum response; bP < 0.01 versus BDL + NS group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4487904&req=5

fig2: Response elicited by NA in rat thoracic aortic rings from NS group, GSH group, BDL + NS group, and BDL + GSH group (n = 6). Data are presented as mean ± SD. aP < 0.01 versus NS group for % maximum response; bP < 0.01 versus BDL + NS group.
Mentions: Cumulative addition of NA (10−9–10−5 mol/L) resulted in concentration dependent contractions in aortas of all groups. The maximum contractile responses to NA (10−8–10−5 mol/L) in the aortas from the NS group rats in the presence of endothelium were significantly (P < 0.01) greater than the BDL + NS group rats. Compared with the BDL + NS group, GSH pretreatment (BDL + GSH group) enhanced contractile response of thoracic aortic rings to NA (3 × 10−8–10−5 mol/L) (Figure 2).

Bottom Line: We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model.The proinflammatory cytokines levels (TNF-α and IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well.All of those were reduced by the treatment of GSH.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesia & Intensive Care, Eastern Hepatobiliary Surgery Hospital, the Second Military Medical University, Shanghai 200438, China ; Department of Anesthesiology, 81st Hospital of the Chinese PLA, Nanjing 210002, China.

ABSTRACT
We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: a NS group, a GSH group, a BDL + NS group, and a BDL + GSH group. GSH was administrated into rats in the GSH and BDL + GSH groups by gastric gavage. An equal volume of normal saline was, respectively, given in the NS group and BDL + NS group. Blood was gathered for serological determination and thoracic aorta rings were isolated for measurement of isometric tension. Obstructive jaundice led to a significant increase in the serum total bilirubin, AST, and ALT levels. The proinflammatory cytokines levels (TNF-α and IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well. All of those were reduced by the treatment of GSH. Meanwhile, contraction of aorta rings to NA and vasorelaxation to ACh or SNP in the BDL group rats were markedly decreased, while GSH administration reversed this change. Our findings suggested that GSH supplementation attenuated overexpressed ONOO(-) from the reaction of excessive NO with O2 (∙-) and protected against obstructive jaundice-induced vascular hyporesponsiveness in rats.

No MeSH data available.


Related in: MedlinePlus