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Int J Clin Exp Pathol. 2015 Sep 1;8(9):11503-9. eCollection 2015.

Curcumin prevents the non-alcoholic fatty hepatitis via mitochondria protection and apoptosis reduction.

Author information

1
Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital 600 Yishan Road, Shanghai 200233, China.
2
Department of Mathematics, Shanghai Jiao Tong University 800 Dongchuan Road, Shanghai 200240, China.

Abstract

BACKGROUND:

Non-alcoholic fatty hepatitis (NASH) is highly prevalent, mitochondria damage is the main pathophysiological characteristic of NASH. However, treatment for mitochondria damage is rarely reported.

METHODS:

NASH model was established in rats, the protective effects of curcumin were evaluated by histological observation; structure and function assessments of mitochondria; and apoptotic genes expression.

RESULTS:

NASH rats treated with curcumin displayed relatively slight liver damage when compared with NASH livers. The average mitochondrial length and width of NASH (12.0 ± 3.2 and 5.1 ± 1.1 micrometers) were significantly longer than that of normal (6.2 ± 2.1 and 2.1 ± 1.5 micrometers) and NASH treated with curcumin (7.4 ± 1.2 and 3.2 ± 1.5 micrometers) rats. The average malondialdehyde (MDA) and 4-hydroxy nonyl alcohol (HNE) levels in liver homogenates of NASH rats (4.23 ± 0.22 and 19.23 ± 2.3 nmol/Ml) were significantly higher than these in normal (1.32 ± 0.12 and 3.52 ± 0.43 nmol/mL) and NASH treated with curcumin (1.74 ± 0.11 and 4.66 ± 0.99 nmol/mL) rats. The expression levels of CytC, Casp3 and Casp8 of the NASH livers were significantly higher than normal and NASH treated with curcumin rats livers.

CONCLUSION:

Our data demonstrated that curcumin prevents the NASH by mitochondria protection and apoptosis reduction and provided a possible novel treatment for NASH.

KEYWORDS:

Curcumin; apoptosis; mitochondria damage; non-alcoholic fatty hepatitis

PMID:
26617882
PMCID:
PMC4637698
[Indexed for MEDLINE]
Free PMC Article

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