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1.  18α-Glycyrrhetinic Acid Down-Regulates Expression of Type I and III Collagen via TGF-Β1/Smad Signaling Pathway in Human and Rat Hepatic Stellate Cells 
Objective: To investigate the effects of 18α-glycyrrhetinic acid (18α-GA) on the expression of type I and III collagen in human and rat hepatic stellate cells (HSC) and to explore the role of TGF-β1/Smad signaling pathway involved.
Methods: Following 18α-GA treatment, the cell viability and cell growth were detected to determine the optimal concentration of 18α-GA. The expressions of TGF-β1/Smad signaling-related genes including type I and III collagen in human and rat HSCs before and after 18α-GA treatment were measured by real time PCR. The expression of related proteins was verified by western blot assay. The phosphorylation level of Smad2 and Smad3 was detected by immunocytochemistry. The DNA binding activities of SP-1, AP-1 and NF-κB were measured by both EMSA and ArrayStar transcription factor activity assay.
Results: 18α-GA could decrease the mRNA and protein expression of Smad3, type I and III collagen, increase the Smad7 expression in human and rat HSCs (P<0.05), and reduce phosphorylation level of Smad3 at 24 h and 48 h after treatment. The DNA binding activities of transcription factors were suppressed by 18α-GA in human and rat HSCs at 24 h, and the activities reduced in a time dependent manner with the lowest activities at 48 h, especially for SP-1.
Conclusion: 18α-GA could inhibit the mRNA and protein expression of type I and III collagen in human and rat HSCs, which may be attributed to down-regulation of Smad3, up-regulation of Smad7, and inhibition of DNA binding activities of SP-1, AP-1 and NF-κB.
doi:10.7150/ijms.4395
PMCID: PMC3399217  PMID: 22811611
18α-glycyrrhetinic acid; hepatic stellate cell; TGF-β1/Smad; transcription factor
2.  18α-Glycyrrhizin induces apoptosis and suppresses activation of rat hepatic stellate cells 
Summary
Background
To investigate the potential mechanisms underlying the protective effects of 18α Glycyrrhizin (GL) on rat hepatic stellate cells (HSCs) and hepatocytes in vivo and in vitro.
Material/Methods
Sprague-Dawley (SD) rats were randomly divided into 5 groups: normal control group, liver fibrosis group, high-dose 18α GL group (25 mg/kg/d), intermediate-dose 18α GL group (12.5 mg/kg/d) and low-dose 18α GL group (6.25 mg/kg/d). The rat liver fibrosis model was induced by carbon tetrachloride (CCl4). The expressions of α-smooth muscle actin (αSMA) and NF-κB were determined by real-time PCR and immunohistochemistry.
Results
18αGL dose-dependently inhibited the CCl4-induced liver fibrosis. There were significant differences in the mRNA and protein expressions of αSMA between the fibrosis group and 18α-GL treatment groups, suggesting that 18α GL can suppress the proliferation and activation of HSCs. Few HSCs were apoptotic in the portal area and fibrous septum in the liver fibrosis group. However, the double-color staining of a-SMA and TUNEL showed that 18α-GL treatment groups increased HSC apoptosis. NF-κB was mainly found in the nucleus in the fibrosis group, while cytoplasmic expression of NF-κB was noted in the 18αGL groups. In the in vitro experiments, 18α GL promoted the proliferation of hepatocytes, but inhibited that of HSCs. HSCs were arrested in the G2/M phase following 18α GL treatment and were largely apoptotic.
Conclusions
18α-GL can suppress the activation of HSCs and induce the apoptosis of HSCs by blocking the translocation of NF-κB into the nucleus, which plays an important role in the protective effect of 18α-GL on liver fibrosis.
doi:10.12659/MSM.882196
PMCID: PMC3560665  PMID: 22207106
18α-glycyrrhizin; hepatocyte; hepatic stellate cell; proliferation; apoptosis
3.  1-(2-Furylmethyl­ene)-2-(2-nitro­phen­yl)hydrazine 
The title Schiff base compound, C11H9N3O3, was obtained from a condensation reaction of furan-2-carbaldehyde and 2-nitro­phenyl­hydrazine. The mol­ecule is roughly planar, the largest deviation from the mean plane defined by all non-H atoms being 0.097 (4). An in ntra­molecular N—H⋯O hydrogen bond might influence the planar conformation of the mol­ecule. In the crystal, weak C—H⋯O hydrogen bonds link the mol­ecules, forming a chain.
doi:10.1107/S1600536809037052
PMCID: PMC2970195  PMID: 21577978

Results 1-3 (3)