The antiapoptotic effects of different doses of β-carotene in chronic ethanol-fed rats

Hsiang Chi Peng, Ya Ling Chen, Shin-Yi Yang, Pei Yin Ho, Sien Sing Yang, Jui-Ting Hu, Suh-Ching Yang

Research output: Contribution to journalArticle

Abstract

BACKGROUND: Ethanol consumption might induce hepatic apoptosis and cause liver damage. The study was to investigate the effects of different doses of β-carotene supplementation on the antioxidant capacity and hepatic apoptosis in chronic ethanol-fed rats.

METHODS: Rats were divided into 6 groups: C (control liquid diet), CLB [control liquid diet with β-carotene supplementation at 0.52 mg/kg body weight (BW)/day], CHB (control liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day), E (ethanol liquid diet), ELB (ethanol liquid diet with β-carotene supplementation at 0.52 mg/kg BW/day), and EHB (ethanol liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day). After 12 weeks, rats were sacrificed and blood and liver samples were collected for analysis.

RESULTS: Lipid peroxidation and hepatic cytochrome P450 2E1 (CYP2E1) expression had increased, and hepatic Fas ligand, caspase-8, cytochrome c, caspase-9, and -3 expressions had significantly increased in the E group. However, lipid peroxidation and CYP2E1, caspase-9, and -3 expressions were significantly lower and Bcl-xL expression was higher in the ELB group. The hepatic tumor necrosis factor (TNF)-α level, lipid peroxidation, and cytochrome c expression were significantly lower and Bcl-2 expression was significantly higher in the EHB group.

CONCLUSIONS: The results suggest that ethanol treatment causes oxidative stress and hepatic apoptosis leading to liver injury, and β-carotene supplementation (0.52 mg/kg BW/day) can prevent ethanol-induced liver damage by decreasing ethanol-induced oxidative stress and inhibiting apoptosis in the liver.

Original languageEnglish
Pages (from-to)132-41
Number of pages10
JournalHepatobiliary surgery and nutrition
Volume2
Issue number3
DOIs
Publication statusPublished - Jun 2013

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Carotenoids
Ethanol
Liver
Diet
Body Weight
Apoptosis
Lipid Peroxidation
Cytochrome P-450 CYP2E1
Caspase 9
Cytochromes c
Caspase 3
Oxidative Stress
Fas Ligand Protein
Caspase 8
Tumor Necrosis Factor-alpha
Antioxidants
Control Groups

Keywords

  • Alcoholic liver disease (ALD)
  • antioxidative stress
  • apoptosis
  • rat
  • β-carotene

Cite this

The antiapoptotic effects of different doses of β-carotene in chronic ethanol-fed rats. / Peng, Hsiang Chi; Chen, Ya Ling; Yang, Shin-Yi; Ho, Pei Yin; Yang, Sien Sing; Hu, Jui-Ting; Yang, Suh-Ching.

In: Hepatobiliary surgery and nutrition, Vol. 2, No. 3, 06.2013, p. 132-41.

Research output: Contribution to journalArticle

Peng, Hsiang Chi ; Chen, Ya Ling ; Yang, Shin-Yi ; Ho, Pei Yin ; Yang, Sien Sing ; Hu, Jui-Ting ; Yang, Suh-Ching. / The antiapoptotic effects of different doses of β-carotene in chronic ethanol-fed rats. In: Hepatobiliary surgery and nutrition. 2013 ; Vol. 2, No. 3. pp. 132-41.
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abstract = "BACKGROUND: Ethanol consumption might induce hepatic apoptosis and cause liver damage. The study was to investigate the effects of different doses of β-carotene supplementation on the antioxidant capacity and hepatic apoptosis in chronic ethanol-fed rats.METHODS: Rats were divided into 6 groups: C (control liquid diet), CLB [control liquid diet with β-carotene supplementation at 0.52 mg/kg body weight (BW)/day], CHB (control liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day), E (ethanol liquid diet), ELB (ethanol liquid diet with β-carotene supplementation at 0.52 mg/kg BW/day), and EHB (ethanol liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day). After 12 weeks, rats were sacrificed and blood and liver samples were collected for analysis.RESULTS: Lipid peroxidation and hepatic cytochrome P450 2E1 (CYP2E1) expression had increased, and hepatic Fas ligand, caspase-8, cytochrome c, caspase-9, and -3 expressions had significantly increased in the E group. However, lipid peroxidation and CYP2E1, caspase-9, and -3 expressions were significantly lower and Bcl-xL expression was higher in the ELB group. The hepatic tumor necrosis factor (TNF)-α level, lipid peroxidation, and cytochrome c expression were significantly lower and Bcl-2 expression was significantly higher in the EHB group.CONCLUSIONS: The results suggest that ethanol treatment causes oxidative stress and hepatic apoptosis leading to liver injury, and β-carotene supplementation (0.52 mg/kg BW/day) can prevent ethanol-induced liver damage by decreasing ethanol-induced oxidative stress and inhibiting apoptosis in the liver.",
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AU - Peng, Hsiang Chi

AU - Chen, Ya Ling

AU - Yang, Shin-Yi

AU - Ho, Pei Yin

AU - Yang, Sien Sing

AU - Hu, Jui-Ting

AU - Yang, Suh-Ching

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N2 - BACKGROUND: Ethanol consumption might induce hepatic apoptosis and cause liver damage. The study was to investigate the effects of different doses of β-carotene supplementation on the antioxidant capacity and hepatic apoptosis in chronic ethanol-fed rats.METHODS: Rats were divided into 6 groups: C (control liquid diet), CLB [control liquid diet with β-carotene supplementation at 0.52 mg/kg body weight (BW)/day], CHB (control liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day), E (ethanol liquid diet), ELB (ethanol liquid diet with β-carotene supplementation at 0.52 mg/kg BW/day), and EHB (ethanol liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day). After 12 weeks, rats were sacrificed and blood and liver samples were collected for analysis.RESULTS: Lipid peroxidation and hepatic cytochrome P450 2E1 (CYP2E1) expression had increased, and hepatic Fas ligand, caspase-8, cytochrome c, caspase-9, and -3 expressions had significantly increased in the E group. However, lipid peroxidation and CYP2E1, caspase-9, and -3 expressions were significantly lower and Bcl-xL expression was higher in the ELB group. The hepatic tumor necrosis factor (TNF)-α level, lipid peroxidation, and cytochrome c expression were significantly lower and Bcl-2 expression was significantly higher in the EHB group.CONCLUSIONS: The results suggest that ethanol treatment causes oxidative stress and hepatic apoptosis leading to liver injury, and β-carotene supplementation (0.52 mg/kg BW/day) can prevent ethanol-induced liver damage by decreasing ethanol-induced oxidative stress and inhibiting apoptosis in the liver.

AB - BACKGROUND: Ethanol consumption might induce hepatic apoptosis and cause liver damage. The study was to investigate the effects of different doses of β-carotene supplementation on the antioxidant capacity and hepatic apoptosis in chronic ethanol-fed rats.METHODS: Rats were divided into 6 groups: C (control liquid diet), CLB [control liquid diet with β-carotene supplementation at 0.52 mg/kg body weight (BW)/day], CHB (control liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day), E (ethanol liquid diet), ELB (ethanol liquid diet with β-carotene supplementation at 0.52 mg/kg BW/day), and EHB (ethanol liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day). After 12 weeks, rats were sacrificed and blood and liver samples were collected for analysis.RESULTS: Lipid peroxidation and hepatic cytochrome P450 2E1 (CYP2E1) expression had increased, and hepatic Fas ligand, caspase-8, cytochrome c, caspase-9, and -3 expressions had significantly increased in the E group. However, lipid peroxidation and CYP2E1, caspase-9, and -3 expressions were significantly lower and Bcl-xL expression was higher in the ELB group. The hepatic tumor necrosis factor (TNF)-α level, lipid peroxidation, and cytochrome c expression were significantly lower and Bcl-2 expression was significantly higher in the EHB group.CONCLUSIONS: The results suggest that ethanol treatment causes oxidative stress and hepatic apoptosis leading to liver injury, and β-carotene supplementation (0.52 mg/kg BW/day) can prevent ethanol-induced liver damage by decreasing ethanol-induced oxidative stress and inhibiting apoptosis in the liver.

KW - Alcoholic liver disease (ALD)

KW - antioxidative stress

KW - apoptosis

KW - rat

KW - β-carotene

U2 - 10.3978/j.issn.2304-3881.2013.06.08

DO - 10.3978/j.issn.2304-3881.2013.06.08

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VL - 2

SP - 132

EP - 141

JO - Hepatobiliary surgery and nutrition

JF - Hepatobiliary surgery and nutrition

SN - 2304-3881

IS - 3

ER -