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Eugenol-rich Fraction of Syzygium aromaticum (Clove) Reverses Biochemical and Histopathological Changes in Liver Cirrhosis and Inhibits Hepatic Cell Proliferation.

Ali S, Prasad R, Mahmood A, Routray I, Shinkafi TS, Sahin K, Kucuk O - J Cancer Prev (2014)

Bottom Line: Histopathology of the liver corroborated the effect of ERF with biochemical findings.ERF treatment further inhibited cell proliferation, as demonstrated by reduced [(3)H]-thymidine uptake.The study assumes significance because cirrhosis predisposes the liver to cancer, which is characterized by abnormal cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Science, Jamia Hamdard, Hamdard Nagar, New Delhi, India.

ABSTRACT

Background: Dried flower bud of Syzygium aromaticum (clove) is rich in eugenol, an antioxidant and antiinflammatory compound that can protect liver against injury. Clove, besides eugenol, also contains other pharmacologically active phytochemicals such as β-sitosterol and ascorbic acid. This study reports the effect of eugenol-rich fraction (ERF) of clove on liver cirrhosis induced by thioacetamide.

Methods: Cirrhosis of the liver, which predisposes to hepatocellular carcinoma, was induced by administering thioacetamide (0.03%) in drinking water for 16 weeks. Cirrhotic animals were divided into two groups; the treated group was administered ERF for 9 weeks, one week after discontinuation of thioacetamide, while the other group received normal saline for a similar duration of time.

Results: The treatment with ERF, as determined by histopathology and through a battery of biochemical markers of hepatic injury, oxidative stress and drug metabolizing enzymes, significantly ameliorated the signs of liver cirrhosis. It lowered the elevated levels of alkaline phosphatase, γ-glutamyl transferase and other biochemical changes in liver cirrhosis. Histopathology of the liver corroborated the effect of ERF with biochemical findings. ERF treatment further inhibited cell proliferation, as demonstrated by reduced [(3)H]-thymidine uptake.

Conclusions: Data provide evidence supporting the protective action of ERF on liver cirrhosis. The study assumes significance because cirrhosis predisposes the liver to cancer, which is characterized by abnormal cell proliferation. ERF in this study is reported to inhibit hepatic cell proliferation and at the same time decrease oxidative stress, which might be the mechanism of protection against liver cirrhosis.

No MeSH data available.


Related in: MedlinePlus

(A) Hepatic lipid peroxidation (LPO) and glutathione (GSH); values are shown as percent of control. Activity of (B) hepatic glutathione reductase, (C) glutathione peroxidase, (D) catalase, (E) succinate dehydrogenase, (F) xanthine oxidase, and (G) glutathione S-transferase. Data represent mean ± SE (n = 5). *P < 0.01, **P < 0.03, when compared with cirrhotic animals. NC, normal control; SA, ERF-treated control; LC, liver cirrhosis; T, ERF-treated liver cirrhosis.
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f4-jcp-19-288: (A) Hepatic lipid peroxidation (LPO) and glutathione (GSH); values are shown as percent of control. Activity of (B) hepatic glutathione reductase, (C) glutathione peroxidase, (D) catalase, (E) succinate dehydrogenase, (F) xanthine oxidase, and (G) glutathione S-transferase. Data represent mean ± SE (n = 5). *P < 0.01, **P < 0.03, when compared with cirrhotic animals. NC, normal control; SA, ERF-treated control; LC, liver cirrhosis; T, ERF-treated liver cirrhosis.

Mentions: LPO is a prominent feature in rats with cirrhosis (Fig. 4A). The increase in LPO was accompanied by a concomitant decrease in glutathione, which indicate oxidative stress, an important factor for the development of liver fibrosis and cirrhosis. ERF significantly decreased elevated LPO in the whole liver homogenate and increased glutathione (Fig. 4A). The activity of GR, enzyme involved in glutathione metabolism, was found to be decreased in liver cirrhosis (Fig. 4B). Glutathione peroxidase (Fig. 4C) and catalase (Fig. 4D), the two enzymes involved in peroxide metabolism, were also decreased in this group, as was the SDH (Fig. 4E). ERF significantly increased the activity level of these enzymes. In cirrhotic rats, there was an increase in activity of XO and GST, the two enzymes involved in drug metabolism (Fig. 4F and 4G). Both of these enzymes were significantly low in ERF treated rats when compared with cirrhotic animals.


Eugenol-rich Fraction of Syzygium aromaticum (Clove) Reverses Biochemical and Histopathological Changes in Liver Cirrhosis and Inhibits Hepatic Cell Proliferation.

Ali S, Prasad R, Mahmood A, Routray I, Shinkafi TS, Sahin K, Kucuk O - J Cancer Prev (2014)

(A) Hepatic lipid peroxidation (LPO) and glutathione (GSH); values are shown as percent of control. Activity of (B) hepatic glutathione reductase, (C) glutathione peroxidase, (D) catalase, (E) succinate dehydrogenase, (F) xanthine oxidase, and (G) glutathione S-transferase. Data represent mean ± SE (n = 5). *P < 0.01, **P < 0.03, when compared with cirrhotic animals. NC, normal control; SA, ERF-treated control; LC, liver cirrhosis; T, ERF-treated liver cirrhosis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4285960&req=5

f4-jcp-19-288: (A) Hepatic lipid peroxidation (LPO) and glutathione (GSH); values are shown as percent of control. Activity of (B) hepatic glutathione reductase, (C) glutathione peroxidase, (D) catalase, (E) succinate dehydrogenase, (F) xanthine oxidase, and (G) glutathione S-transferase. Data represent mean ± SE (n = 5). *P < 0.01, **P < 0.03, when compared with cirrhotic animals. NC, normal control; SA, ERF-treated control; LC, liver cirrhosis; T, ERF-treated liver cirrhosis.
Mentions: LPO is a prominent feature in rats with cirrhosis (Fig. 4A). The increase in LPO was accompanied by a concomitant decrease in glutathione, which indicate oxidative stress, an important factor for the development of liver fibrosis and cirrhosis. ERF significantly decreased elevated LPO in the whole liver homogenate and increased glutathione (Fig. 4A). The activity of GR, enzyme involved in glutathione metabolism, was found to be decreased in liver cirrhosis (Fig. 4B). Glutathione peroxidase (Fig. 4C) and catalase (Fig. 4D), the two enzymes involved in peroxide metabolism, were also decreased in this group, as was the SDH (Fig. 4E). ERF significantly increased the activity level of these enzymes. In cirrhotic rats, there was an increase in activity of XO and GST, the two enzymes involved in drug metabolism (Fig. 4F and 4G). Both of these enzymes were significantly low in ERF treated rats when compared with cirrhotic animals.

Bottom Line: Histopathology of the liver corroborated the effect of ERF with biochemical findings.ERF treatment further inhibited cell proliferation, as demonstrated by reduced [(3)H]-thymidine uptake.The study assumes significance because cirrhosis predisposes the liver to cancer, which is characterized by abnormal cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Science, Jamia Hamdard, Hamdard Nagar, New Delhi, India.

ABSTRACT

Background: Dried flower bud of Syzygium aromaticum (clove) is rich in eugenol, an antioxidant and antiinflammatory compound that can protect liver against injury. Clove, besides eugenol, also contains other pharmacologically active phytochemicals such as β-sitosterol and ascorbic acid. This study reports the effect of eugenol-rich fraction (ERF) of clove on liver cirrhosis induced by thioacetamide.

Methods: Cirrhosis of the liver, which predisposes to hepatocellular carcinoma, was induced by administering thioacetamide (0.03%) in drinking water for 16 weeks. Cirrhotic animals were divided into two groups; the treated group was administered ERF for 9 weeks, one week after discontinuation of thioacetamide, while the other group received normal saline for a similar duration of time.

Results: The treatment with ERF, as determined by histopathology and through a battery of biochemical markers of hepatic injury, oxidative stress and drug metabolizing enzymes, significantly ameliorated the signs of liver cirrhosis. It lowered the elevated levels of alkaline phosphatase, γ-glutamyl transferase and other biochemical changes in liver cirrhosis. Histopathology of the liver corroborated the effect of ERF with biochemical findings. ERF treatment further inhibited cell proliferation, as demonstrated by reduced [(3)H]-thymidine uptake.

Conclusions: Data provide evidence supporting the protective action of ERF on liver cirrhosis. The study assumes significance because cirrhosis predisposes the liver to cancer, which is characterized by abnormal cell proliferation. ERF in this study is reported to inhibit hepatic cell proliferation and at the same time decrease oxidative stress, which might be the mechanism of protection against liver cirrhosis.

No MeSH data available.


Related in: MedlinePlus