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Ruscogenin ameliorates experimental nonalcoholic steatohepatitis via suppressing lipogenesis and inflammatory pathway.

Lu HJ, Tzeng TF, Liou SS, Chang CJ, Yang C, Wu MC, Liu IM - Biomed Res Int (2014)

Bottom Line: Ruscogenin (10.0 μmol/l) had inhibitory effects on PA-induced triglyceride accumulation and inflammatory markers in HepG2 cells.Conversely, ruscogenin decreased expression of genes involved in hepatic lipogenesis.Ruscogenin may attenuate HFD-induced steatohepatitis through downregulation of NF-κB-mediated inflammatory responses, reducing hepatic lipogenic gene expression, and upregulating proteins in β-oxidation pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Food Science, College of Agriculture, National Pingtung University of Science and Technology, Neipu Township, Pingtung County, Taiwan.

ABSTRACT
The aim of the study was to investigate the protective effects of ruscogenin, a major steroid sapogenin in Ophiopogon japonicus, on experimental models of nonalcoholic steatohepatitis. HepG2 cells were exposed to 300 μmol/l palmitic acid (PA) for 24 h with the preincubation of ruscogenin for another 24 h. Ruscogenin (10.0 μmol/l) had inhibitory effects on PA-induced triglyceride accumulation and inflammatory markers in HepG2 cells. Male golden hamsters were randomly divided into five groups fed a normal diet, a high-fat diet (HFD), or a HFD supplemented with ruscogenin (0.3, 1.0, or 3.0 mg/kg/day) by gavage once daily for 8 weeks. Ruscogenin alleviated dyslipidemia, liver steatosis, and necroinflammation and reversed plasma markers of metabolic syndrome in HFD-fed hamsters. Hepatic mRNA levels involved in fatty acid oxidation were increased in ruscogenin-treated HFD-fed hamsters. Conversely, ruscogenin decreased expression of genes involved in hepatic lipogenesis. Gene expression of inflammatory cytokines, chemoattractive mediator, nuclear transcription factor-(NF-) κB, and α-smooth muscle actin were increased in the HFD group, which were attenuated by ruscogenin. Ruscogenin may attenuate HFD-induced steatohepatitis through downregulation of NF-κB-mediated inflammatory responses, reducing hepatic lipogenic gene expression, and upregulating proteins in β-oxidation pathway.

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Related in: MedlinePlus

Representative images of H&E and stained livers from RCD- or HFD-fed hamsters receiving 8 weeks of treatments. Photomicrographs (original magnification, 400x) are of tissues isolated from vehicle-treated RCD-fed hamsters (RCD-vehicle), vehicle-treated HFD-fed hamsters (HFD-vehicle), or ruscogenin (3.0 mg/kg/day) treated HFD-fed hamsters (HFD-ruscogenin). Arrows and arrow head indicate fat droplets and necroinflammatory foci, respectively. The severity of hepatic steatosis and necroinflammation were scored in Table 3.
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fig3: Representative images of H&E and stained livers from RCD- or HFD-fed hamsters receiving 8 weeks of treatments. Photomicrographs (original magnification, 400x) are of tissues isolated from vehicle-treated RCD-fed hamsters (RCD-vehicle), vehicle-treated HFD-fed hamsters (HFD-vehicle), or ruscogenin (3.0 mg/kg/day) treated HFD-fed hamsters (HFD-ruscogenin). Arrows and arrow head indicate fat droplets and necroinflammatory foci, respectively. The severity of hepatic steatosis and necroinflammation were scored in Table 3.

Mentions: Representative histological photomicrographs of liver specimens are shown in Figure 3. Hamsters fed a RCD had normal liver histological findings; however, numerous macrovascular fat droplets and mild necroinflammatory foci were present in livers of those fed a HFD. Treatment of HFD-fed hamsters with ruscogenin (3.0 mg/kg/day) reduced fat liver depots and less macrovesicular steatosis as revealed in vehicle-treated counterparts (Figure 3). Ruscogenin treatment (3.0 mg/kg/day) clearly reduced hepatic necroinflammation (Figure 3). Histological grading of liver sections confirmed that ruscogenin treatment significantly ameliorated both hepatic steatosis and necroinflammation (Table 3).


Ruscogenin ameliorates experimental nonalcoholic steatohepatitis via suppressing lipogenesis and inflammatory pathway.

Lu HJ, Tzeng TF, Liou SS, Chang CJ, Yang C, Wu MC, Liu IM - Biomed Res Int (2014)

Representative images of H&E and stained livers from RCD- or HFD-fed hamsters receiving 8 weeks of treatments. Photomicrographs (original magnification, 400x) are of tissues isolated from vehicle-treated RCD-fed hamsters (RCD-vehicle), vehicle-treated HFD-fed hamsters (HFD-vehicle), or ruscogenin (3.0 mg/kg/day) treated HFD-fed hamsters (HFD-ruscogenin). Arrows and arrow head indicate fat droplets and necroinflammatory foci, respectively. The severity of hepatic steatosis and necroinflammation were scored in Table 3.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4127260&req=5

fig3: Representative images of H&E and stained livers from RCD- or HFD-fed hamsters receiving 8 weeks of treatments. Photomicrographs (original magnification, 400x) are of tissues isolated from vehicle-treated RCD-fed hamsters (RCD-vehicle), vehicle-treated HFD-fed hamsters (HFD-vehicle), or ruscogenin (3.0 mg/kg/day) treated HFD-fed hamsters (HFD-ruscogenin). Arrows and arrow head indicate fat droplets and necroinflammatory foci, respectively. The severity of hepatic steatosis and necroinflammation were scored in Table 3.
Mentions: Representative histological photomicrographs of liver specimens are shown in Figure 3. Hamsters fed a RCD had normal liver histological findings; however, numerous macrovascular fat droplets and mild necroinflammatory foci were present in livers of those fed a HFD. Treatment of HFD-fed hamsters with ruscogenin (3.0 mg/kg/day) reduced fat liver depots and less macrovesicular steatosis as revealed in vehicle-treated counterparts (Figure 3). Ruscogenin treatment (3.0 mg/kg/day) clearly reduced hepatic necroinflammation (Figure 3). Histological grading of liver sections confirmed that ruscogenin treatment significantly ameliorated both hepatic steatosis and necroinflammation (Table 3).

Bottom Line: Ruscogenin (10.0 μmol/l) had inhibitory effects on PA-induced triglyceride accumulation and inflammatory markers in HepG2 cells.Conversely, ruscogenin decreased expression of genes involved in hepatic lipogenesis.Ruscogenin may attenuate HFD-induced steatohepatitis through downregulation of NF-κB-mediated inflammatory responses, reducing hepatic lipogenic gene expression, and upregulating proteins in β-oxidation pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Food Science, College of Agriculture, National Pingtung University of Science and Technology, Neipu Township, Pingtung County, Taiwan.

ABSTRACT
The aim of the study was to investigate the protective effects of ruscogenin, a major steroid sapogenin in Ophiopogon japonicus, on experimental models of nonalcoholic steatohepatitis. HepG2 cells were exposed to 300 μmol/l palmitic acid (PA) for 24 h with the preincubation of ruscogenin for another 24 h. Ruscogenin (10.0 μmol/l) had inhibitory effects on PA-induced triglyceride accumulation and inflammatory markers in HepG2 cells. Male golden hamsters were randomly divided into five groups fed a normal diet, a high-fat diet (HFD), or a HFD supplemented with ruscogenin (0.3, 1.0, or 3.0 mg/kg/day) by gavage once daily for 8 weeks. Ruscogenin alleviated dyslipidemia, liver steatosis, and necroinflammation and reversed plasma markers of metabolic syndrome in HFD-fed hamsters. Hepatic mRNA levels involved in fatty acid oxidation were increased in ruscogenin-treated HFD-fed hamsters. Conversely, ruscogenin decreased expression of genes involved in hepatic lipogenesis. Gene expression of inflammatory cytokines, chemoattractive mediator, nuclear transcription factor-(NF-) κB, and α-smooth muscle actin were increased in the HFD group, which were attenuated by ruscogenin. Ruscogenin may attenuate HFD-induced steatohepatitis through downregulation of NF-κB-mediated inflammatory responses, reducing hepatic lipogenic gene expression, and upregulating proteins in β-oxidation pathway.

Show MeSH
Related in: MedlinePlus