Solanum nigrum protects against hepatic fibrosis via suppression of hyperglycemia in high-fat/ethanol diet-induced rats

Cheng Jeng Tai, Chen Yen Choong, Yeu Ching Shi, Yu Chun Lin, Chia-Woei Wang, Bao Hong Lee, Chen Jei Tai

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background: Advanced glycation end products (AGEs) signal through the receptor for AGE (RAGE), which can lead to hepatic fibrosis in hyperglycemia and hyperlipidemia. We investigated the inhibitory effect of aqueous extracts from Solanum nigrum (AESN) on AGEs-induced RAGE signaling and activation of hepatic stellate cells (HSCs) and hyperglycemia induced by high-fat diet with ethanol. Methods: An animal model was used to evaluate the anti-hepatic fibrosis activity of AESN in rats fed a high-fat diet (HFD; 30%) with ethanol (10%). Male Wistar rats (4 weeks of age) were randomly divided into four groups (n = 6): (1) control (basal diet); (2) HFD (30%) + ethanol (10%) (HFD/ethanol); (3) HFD/ethanol + AESN (100 mg/kg, oral administration); and (4) HFD/ethanol + pioglitazone (10 mg/kg, oral administration) and treated with HFD for 6 months in the presence or absence of 10% ethanol in dietary water. Results: We found that AESN improved insulin resistance and hyperinsulinemia, and downregulated lipogenesis via regulation of the peroxisome proliferator-activated receptor α (PPARα), PPAR co-activator (PGC-1α), carbohydrate response element-binding protein (ChREBP), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) mRNA levels in the liver of HFD/ethanol-treated rats. In turn, AESN may delay and inhibit the progression of hepatic fibrosis, including α-smooth muscle actin (α-SMA) inhibition and MMP-2 production. Conclusions: These results suggest that AESN may be further explored as a novel anti-fibrotic strategy for the prevention of liver disease.

Original languageEnglish
Article number269
JournalMolecules
Volume21
Issue number3
DOIs
Publication statusPublished - Mar 1 2016

Fingerprint

Solanum nigrum
hyperglycemia
fibrosis
diets
fats
High Fat Diet
Nutrition
Hyperglycemia
rats
Rats
Fibrosis
ethyl alcohol
Ethanol
Fats
retarding
Liver
Peroxisome Proliferator-Activated Receptors
pioglitazone
liver
Oral Administration

Keywords

  • Advanced glycation end products (AGEs)
  • Hepatic fibrosis
  • Hyperglycemia
  • Hyperlipidemia
  • Solanum nigrum

ASJC Scopus subject areas

  • Organic Chemistry

Cite this

Solanum nigrum protects against hepatic fibrosis via suppression of hyperglycemia in high-fat/ethanol diet-induced rats. / Tai, Cheng Jeng; Choong, Chen Yen; Shi, Yeu Ching; Lin, Yu Chun; Wang, Chia-Woei; Lee, Bao Hong; Tai, Chen Jei.

In: Molecules, Vol. 21, No. 3, 269, 01.03.2016.

Research output: Contribution to journalArticle

Tai, Cheng Jeng ; Choong, Chen Yen ; Shi, Yeu Ching ; Lin, Yu Chun ; Wang, Chia-Woei ; Lee, Bao Hong ; Tai, Chen Jei. / Solanum nigrum protects against hepatic fibrosis via suppression of hyperglycemia in high-fat/ethanol diet-induced rats. In: Molecules. 2016 ; Vol. 21, No. 3.
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abstract = "Background: Advanced glycation end products (AGEs) signal through the receptor for AGE (RAGE), which can lead to hepatic fibrosis in hyperglycemia and hyperlipidemia. We investigated the inhibitory effect of aqueous extracts from Solanum nigrum (AESN) on AGEs-induced RAGE signaling and activation of hepatic stellate cells (HSCs) and hyperglycemia induced by high-fat diet with ethanol. Methods: An animal model was used to evaluate the anti-hepatic fibrosis activity of AESN in rats fed a high-fat diet (HFD; 30{\%}) with ethanol (10{\%}). Male Wistar rats (4 weeks of age) were randomly divided into four groups (n = 6): (1) control (basal diet); (2) HFD (30{\%}) + ethanol (10{\%}) (HFD/ethanol); (3) HFD/ethanol + AESN (100 mg/kg, oral administration); and (4) HFD/ethanol + pioglitazone (10 mg/kg, oral administration) and treated with HFD for 6 months in the presence or absence of 10{\%} ethanol in dietary water. Results: We found that AESN improved insulin resistance and hyperinsulinemia, and downregulated lipogenesis via regulation of the peroxisome proliferator-activated receptor α (PPARα), PPAR co-activator (PGC-1α), carbohydrate response element-binding protein (ChREBP), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) mRNA levels in the liver of HFD/ethanol-treated rats. In turn, AESN may delay and inhibit the progression of hepatic fibrosis, including α-smooth muscle actin (α-SMA) inhibition and MMP-2 production. Conclusions: These results suggest that AESN may be further explored as a novel anti-fibrotic strategy for the prevention of liver disease.",
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AU - Tai, Cheng Jeng

AU - Choong, Chen Yen

AU - Shi, Yeu Ching

AU - Lin, Yu Chun

AU - Wang, Chia-Woei

AU - Lee, Bao Hong

AU - Tai, Chen Jei

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AB - Background: Advanced glycation end products (AGEs) signal through the receptor for AGE (RAGE), which can lead to hepatic fibrosis in hyperglycemia and hyperlipidemia. We investigated the inhibitory effect of aqueous extracts from Solanum nigrum (AESN) on AGEs-induced RAGE signaling and activation of hepatic stellate cells (HSCs) and hyperglycemia induced by high-fat diet with ethanol. Methods: An animal model was used to evaluate the anti-hepatic fibrosis activity of AESN in rats fed a high-fat diet (HFD; 30%) with ethanol (10%). Male Wistar rats (4 weeks of age) were randomly divided into four groups (n = 6): (1) control (basal diet); (2) HFD (30%) + ethanol (10%) (HFD/ethanol); (3) HFD/ethanol + AESN (100 mg/kg, oral administration); and (4) HFD/ethanol + pioglitazone (10 mg/kg, oral administration) and treated with HFD for 6 months in the presence or absence of 10% ethanol in dietary water. Results: We found that AESN improved insulin resistance and hyperinsulinemia, and downregulated lipogenesis via regulation of the peroxisome proliferator-activated receptor α (PPARα), PPAR co-activator (PGC-1α), carbohydrate response element-binding protein (ChREBP), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) mRNA levels in the liver of HFD/ethanol-treated rats. In turn, AESN may delay and inhibit the progression of hepatic fibrosis, including α-smooth muscle actin (α-SMA) inhibition and MMP-2 production. Conclusions: These results suggest that AESN may be further explored as a novel anti-fibrotic strategy for the prevention of liver disease.

KW - Advanced glycation end products (AGEs)

KW - Hepatic fibrosis

KW - Hyperglycemia

KW - Hyperlipidemia

KW - Solanum nigrum

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