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Ginseng extract and ginsenoside Rb1 attenuate carbon tetrachloride-induced liver fibrosis in rats.

Hou YL, Tsai YH, Lin YH, Chao JC - BMC Complement Altern Med (2014)

Bottom Line: Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities.The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4.Both Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E2, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1β concentrations (p <0.05).

View Article: PubMed Central - PubMed

Affiliation: School of Nutrition and Health Sciences, College of Public Health and Nutrition, Taipei Medical University, Taipei 110, Taiwan. chenjui@tmu.edu.tw.

ABSTRACT

Background: Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities. This study investigated the effects of ginsenosides on carbon tetrachloride (CCl4)-induced hepatitis and liver fibrosis in rats.

Methods: Male Sprague-Dawley rats were randomly divided into four groups: control, CCl4, CCl4 + 0.5 g/kg Panax ginseng extract and CCl4 + 0.05 g/kg ginsenoside Rb1 groups. The treated groups were orally given Panax ginseng extract or ginsenoside Rb1 two weeks before the induction of liver injury for successive 9 weeks. Liver injury was induced by intraperitoneally injected with 400 ml/l CCl4 at a dose of 0.75 ml/kg body weight weekly for 7 weeks. The control group was intraperitoneally injected with olive oil.

Results: The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4. Plasma alanine aminotransferase and aspartate aminotransferase activities were increased by CCl4 (p <0.01), and aspartate aminotransferase activity was decreased by Panax ginseng extract at week 9 (p <0.05). Exposure to CCl4 for 7 weeks, the levels of plasma and hepatic triglycerides (p <0.01), hepatic cholesterol (p <0.01), interleukin-1β (p <0.01), prostaglandin E2 (p <0.05), soluble intercellular adhesion molecule-1 (p <0.05), hydroxyproline (p <0.05), matrix metalloproteinase-2 (p <0.05) and tissue inhibitor of metalloproteinase-1 (TIMP-1) (p <0.01) were elevated, however, hepatic interleukin-10 level was lowered (p <0.05). Both Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E2, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1β concentrations (p <0.05).

Conclusions: Panax ginseng extract and ginsenoside Rb1 attenuate plasma aminotransferase activities and liver inflammation to inhibit CCl4-induced liver fibrosis through down-regulation of hepatic prostaglandin E2 and TIMP-1.

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The representative histological sections of rat liver specimens. A: Masson’s trichrome stain at 15 × 10 magnification, B: silver stain at 15 × 10 magnification; C: semi-quantitative scores graded from 0 (no collagen formation), 1 (collagen formation in the central vein area), 2 (collagen and fibrous bridge formation in different central vein areas) to 3 (cirrhosis) for fibrosis in the control, CCl4, GE and Rb1 groups. Collagen fibers stained with Masson’s trichrome appear blue. Reticular fibers stained with silver appear brown. Solid and dashed arrows represent the central vein and fiber bridging. Data are presented as mean ± SD (n =10). Values not sharing the same letter differ significantly (p <0.05). Scale bar =50 μm.
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Fig2: The representative histological sections of rat liver specimens. A: Masson’s trichrome stain at 15 × 10 magnification, B: silver stain at 15 × 10 magnification; C: semi-quantitative scores graded from 0 (no collagen formation), 1 (collagen formation in the central vein area), 2 (collagen and fibrous bridge formation in different central vein areas) to 3 (cirrhosis) for fibrosis in the control, CCl4, GE and Rb1 groups. Collagen fibers stained with Masson’s trichrome appear blue. Reticular fibers stained with silver appear brown. Solid and dashed arrows represent the central vein and fiber bridging. Data are presented as mean ± SD (n =10). Values not sharing the same letter differ significantly (p <0.05). Scale bar =50 μm.

Mentions: The results of the histopathological examination by different stains were demonstrated in Figures 1 and 2 to determine the effects of the treatments on histopathological changes in the liver, especially on liver fibrosis. The bright red color of H&E staining shown in Figure 1A could be resulted from strong eosin staining, a fluorescent red dye. The pathological sections stained by H&E showed that no fat was accumulated in the liver of the control group, whereas large fat vacuoles were observed in the liver of the CCl4 group (Figure 1A). However, the Rb1 group had significantly decreased fat vacuoles compared with the CCl4 group (2.65 ± 0.82 vs. 3.50 ± 0.75, p <0.05) (Figure 1B). The pathological scores for fat change were not significantly different between the GE and Rb1 groups. The CCl4, GE, and Rb1 groups had significantly elevated cell necrosis (p <0.05), inflammatory cells (p <0.01), and fibrosis (p <0.01) in the central veins compared with the control group. However, the pathological scores for necrosis, inflammation, and fibrosis in the liver did not significantly differ among the three CCl4 treated groups.Figure 1


Ginseng extract and ginsenoside Rb1 attenuate carbon tetrachloride-induced liver fibrosis in rats.

Hou YL, Tsai YH, Lin YH, Chao JC - BMC Complement Altern Med (2014)

The representative histological sections of rat liver specimens. A: Masson’s trichrome stain at 15 × 10 magnification, B: silver stain at 15 × 10 magnification; C: semi-quantitative scores graded from 0 (no collagen formation), 1 (collagen formation in the central vein area), 2 (collagen and fibrous bridge formation in different central vein areas) to 3 (cirrhosis) for fibrosis in the control, CCl4, GE and Rb1 groups. Collagen fibers stained with Masson’s trichrome appear blue. Reticular fibers stained with silver appear brown. Solid and dashed arrows represent the central vein and fiber bridging. Data are presented as mean ± SD (n =10). Values not sharing the same letter differ significantly (p <0.05). Scale bar =50 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4216840&req=5

Fig2: The representative histological sections of rat liver specimens. A: Masson’s trichrome stain at 15 × 10 magnification, B: silver stain at 15 × 10 magnification; C: semi-quantitative scores graded from 0 (no collagen formation), 1 (collagen formation in the central vein area), 2 (collagen and fibrous bridge formation in different central vein areas) to 3 (cirrhosis) for fibrosis in the control, CCl4, GE and Rb1 groups. Collagen fibers stained with Masson’s trichrome appear blue. Reticular fibers stained with silver appear brown. Solid and dashed arrows represent the central vein and fiber bridging. Data are presented as mean ± SD (n =10). Values not sharing the same letter differ significantly (p <0.05). Scale bar =50 μm.
Mentions: The results of the histopathological examination by different stains were demonstrated in Figures 1 and 2 to determine the effects of the treatments on histopathological changes in the liver, especially on liver fibrosis. The bright red color of H&E staining shown in Figure 1A could be resulted from strong eosin staining, a fluorescent red dye. The pathological sections stained by H&E showed that no fat was accumulated in the liver of the control group, whereas large fat vacuoles were observed in the liver of the CCl4 group (Figure 1A). However, the Rb1 group had significantly decreased fat vacuoles compared with the CCl4 group (2.65 ± 0.82 vs. 3.50 ± 0.75, p <0.05) (Figure 1B). The pathological scores for fat change were not significantly different between the GE and Rb1 groups. The CCl4, GE, and Rb1 groups had significantly elevated cell necrosis (p <0.05), inflammatory cells (p <0.01), and fibrosis (p <0.01) in the central veins compared with the control group. However, the pathological scores for necrosis, inflammation, and fibrosis in the liver did not significantly differ among the three CCl4 treated groups.Figure 1

Bottom Line: Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities.The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4.Both Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E2, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1β concentrations (p <0.05).

View Article: PubMed Central - PubMed

Affiliation: School of Nutrition and Health Sciences, College of Public Health and Nutrition, Taipei Medical University, Taipei 110, Taiwan. chenjui@tmu.edu.tw.

ABSTRACT

Background: Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities. This study investigated the effects of ginsenosides on carbon tetrachloride (CCl4)-induced hepatitis and liver fibrosis in rats.

Methods: Male Sprague-Dawley rats were randomly divided into four groups: control, CCl4, CCl4 + 0.5 g/kg Panax ginseng extract and CCl4 + 0.05 g/kg ginsenoside Rb1 groups. The treated groups were orally given Panax ginseng extract or ginsenoside Rb1 two weeks before the induction of liver injury for successive 9 weeks. Liver injury was induced by intraperitoneally injected with 400 ml/l CCl4 at a dose of 0.75 ml/kg body weight weekly for 7 weeks. The control group was intraperitoneally injected with olive oil.

Results: The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4. Plasma alanine aminotransferase and aspartate aminotransferase activities were increased by CCl4 (p <0.01), and aspartate aminotransferase activity was decreased by Panax ginseng extract at week 9 (p <0.05). Exposure to CCl4 for 7 weeks, the levels of plasma and hepatic triglycerides (p <0.01), hepatic cholesterol (p <0.01), interleukin-1β (p <0.01), prostaglandin E2 (p <0.05), soluble intercellular adhesion molecule-1 (p <0.05), hydroxyproline (p <0.05), matrix metalloproteinase-2 (p <0.05) and tissue inhibitor of metalloproteinase-1 (TIMP-1) (p <0.01) were elevated, however, hepatic interleukin-10 level was lowered (p <0.05). Both Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E2, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1β concentrations (p <0.05).

Conclusions: Panax ginseng extract and ginsenoside Rb1 attenuate plasma aminotransferase activities and liver inflammation to inhibit CCl4-induced liver fibrosis through down-regulation of hepatic prostaglandin E2 and TIMP-1.

Show MeSH
Related in: MedlinePlus