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Vitamin A supplementation alleviates extrahepatic cholestasis liver injury through Nrf2 activation.

Wang G, Xiu P, Li F, Xin C, Li K - Oxid Med Cell Longev (2014)

Bottom Line: Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice.Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1.Vitamin A was here found to ameliorate cholestatic liver injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.

ABSTRACT

Aim: To investigate the role of vitamin A in liver damage induced by bile duct ligation (BDL) in rats.

Methods: Thirty male Wistar rats were randomly divided into three groups: SHAM group, BDL group, and BDL + VitA group . The concentrations of retinol and retinyl palmitate in the liver were analyzed using HPLC, and liver function was evaluated by the level of TBIL, ALT, AST, and ALP in serum. Hepatic oxidative status was estimated by measuring T-SOD, CAT, GSH, MDA, and AOPP. Nrf2 expression was assessed using immunohistochemistry and western blotting, and EMSA was performed to determine Nrf2 DNA-binding activity. The expression of the downstream factors such as Ho1 and Nqo1 was also examined using immunohistochemistry and western blotting assays.

Results: Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice. Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1.

Conclusion: Vitamin A was here found to ameliorate cholestatic liver injury. This effect may be related to the activation of Nrf2/ARE pathway in bile duct ligation rats.

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Related in: MedlinePlus

Levels of TBIL, ALT, AST, and ALP in serum. A: SHAM group (n = 10); B: BDL (n = 8); B: BDL + vitA group (n = 9). Data are presented as mean ± SD. aP < 0.05 versus SHAM group; bP < 0.05 versus BDL group.
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fig3: Levels of TBIL, ALT, AST, and ALP in serum. A: SHAM group (n = 10); B: BDL (n = 8); B: BDL + vitA group (n = 9). Data are presented as mean ± SD. aP < 0.05 versus SHAM group; bP < 0.05 versus BDL group.

Mentions: The serum concentrations of TBIL, ALT, AST, and ALP in BDL group increased visibly compared with those in SHAM group (TBIL: 260.07 ± 28.32 μmol/L versus 3.92 ± 1.43 μmol/L, P < 0.05; ALT: 240.86 ± 52.41 U/L versus 68.77 ± 15.04 U/L, P < 0.05; AST: 691.68 ± 65.45 U/L versus 138.59 ± 38.40 U/L, P < 0.05; ALP: 1029.14 ± 108.40 U/L versus 331.50 ± 40.71 U/L, P < 0.05; Figure 3). The serum concentrations of TBIL, ALT, AST, and ALP were significantly lower in the BDL + vitA group (TBIL: 211.46 ± 19.83 μmol/L versus 260.07 ± 28.32 μmol/L, P < 0.05; ALT: 147.54 ± 22.97 U/L versus 240.86 ± 52.41 U/L, P < 0.05; AST: 370.71 ± 75.30 U/L versus 691.68 ± 65.45 U/L, P < 0.05; ALP: 669.60 ± 65.65 U/L versus 1029.14 ± 108.40 U/L U/L, P < 0.05; Figure 3).


Vitamin A supplementation alleviates extrahepatic cholestasis liver injury through Nrf2 activation.

Wang G, Xiu P, Li F, Xin C, Li K - Oxid Med Cell Longev (2014)

Levels of TBIL, ALT, AST, and ALP in serum. A: SHAM group (n = 10); B: BDL (n = 8); B: BDL + vitA group (n = 9). Data are presented as mean ± SD. aP < 0.05 versus SHAM group; bP < 0.05 versus BDL group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4120926&req=5

fig3: Levels of TBIL, ALT, AST, and ALP in serum. A: SHAM group (n = 10); B: BDL (n = 8); B: BDL + vitA group (n = 9). Data are presented as mean ± SD. aP < 0.05 versus SHAM group; bP < 0.05 versus BDL group.
Mentions: The serum concentrations of TBIL, ALT, AST, and ALP in BDL group increased visibly compared with those in SHAM group (TBIL: 260.07 ± 28.32 μmol/L versus 3.92 ± 1.43 μmol/L, P < 0.05; ALT: 240.86 ± 52.41 U/L versus 68.77 ± 15.04 U/L, P < 0.05; AST: 691.68 ± 65.45 U/L versus 138.59 ± 38.40 U/L, P < 0.05; ALP: 1029.14 ± 108.40 U/L versus 331.50 ± 40.71 U/L, P < 0.05; Figure 3). The serum concentrations of TBIL, ALT, AST, and ALP were significantly lower in the BDL + vitA group (TBIL: 211.46 ± 19.83 μmol/L versus 260.07 ± 28.32 μmol/L, P < 0.05; ALT: 147.54 ± 22.97 U/L versus 240.86 ± 52.41 U/L, P < 0.05; AST: 370.71 ± 75.30 U/L versus 691.68 ± 65.45 U/L, P < 0.05; ALP: 669.60 ± 65.65 U/L versus 1029.14 ± 108.40 U/L U/L, P < 0.05; Figure 3).

Bottom Line: Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice.Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1.Vitamin A was here found to ameliorate cholestatic liver injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.

ABSTRACT

Aim: To investigate the role of vitamin A in liver damage induced by bile duct ligation (BDL) in rats.

Methods: Thirty male Wistar rats were randomly divided into three groups: SHAM group, BDL group, and BDL + VitA group . The concentrations of retinol and retinyl palmitate in the liver were analyzed using HPLC, and liver function was evaluated by the level of TBIL, ALT, AST, and ALP in serum. Hepatic oxidative status was estimated by measuring T-SOD, CAT, GSH, MDA, and AOPP. Nrf2 expression was assessed using immunohistochemistry and western blotting, and EMSA was performed to determine Nrf2 DNA-binding activity. The expression of the downstream factors such as Ho1 and Nqo1 was also examined using immunohistochemistry and western blotting assays.

Results: Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice. Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1.

Conclusion: Vitamin A was here found to ameliorate cholestatic liver injury. This effect may be related to the activation of Nrf2/ARE pathway in bile duct ligation rats.

Show MeSH
Related in: MedlinePlus