Inhibitory effect of schisandrin B on free fatty acid-induced steatosis in L-02 cells

AIM:To investigate the effects of schisandrin B (Sch B) on free fatty acid (FFA)-induced steatosis in L-02 cells.METHODS:Cellular steatosis was induced by incubating L-02 cells with a FFA mixture (oleate and palmitate at the ratio of 2:1) for 24 h.Cytotoxicity and apoptosis were evaluated by 3-(4,5-dmethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and Annexin V/propidium iodide staining,respectively.Cellular total lipid was determined using a photocolorimetric method after Nile red staining,and triglyceride content was measured using an enzymatic kit.To study the effects of Sch B on steatosis,L-02 cells were treated with Sch B (1-100 μmol/L) in the absence or presence of 1 mmol/L FFA for 24 h,and cellular total lipid and triglyceride levels were measured.To explore the mechanisms of action of Sch B in the steatotic L-02 cells,mRNA levels of several regulators of hepatic lipid metabolism including adipose differentiation related protein (ADRP),sterol regulatory element binding protein 1 (SREBP-1),peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ were measured by quantitative real-time polymerase chain reaction (PCR),and protein levels of ADRP and SREBP-1 were measured by immunoblotting.RESULTS:Treatment with 1 mmol/L FFA for 24 h induced intracellular lipid accumulation in L-02 cells comparable to that in human steatotic livers without causing apparent apoptosis and cytotoxicity.Sch B mitigated cellular total lipid and triglyceride accumulations in the steatotic L-02 cells in a dose-dependent manner.Quantitative real-time PCR and Western blot analyses revealed that treatment of L-02 cells with 100 μmol/L Sch B reverted the FFA-stimulated up-regulation of ADRP and SREBP-1.CONCLUSION:Sch B inhibits FFA-induced steatosis in L-02 cells by,at least in part,reversing the up-regulation of ADRP and SREBP-1.

Schisandrae Fructus oil-induced elevation in serum triglyceride and lipoprotein concentrations associated with physiologic hepatomegaly in mice

Objective:To investigate hypertriglyceridemia and hepatomegaly caused by Schisandrae Sphenantherae Fructus(FSS)and Schisandra chinensis Fructus(FSC)oils in mice.Methods:Mice were orally administered a single dose of SchisandraeFructusoils.Serumandhepatictriglyceride(TG),triglyceridetransferprotein(TTP),apolipoproteinB48(Apo B48),very-low-densitylipoprotein(VLDL),hepatocytegrowth factor(HGF),alanine aminotransfease(ALT)and liver index were measured at 6-120 h post-dosing.Results:FSS and FSC oil caused time and dose-dependent increases in serum and hepatic TG levels,with maximum increases in the liver(by 297%and 340%)at 12 h post-dosing and serum(244%and 439%)at 24-h post-dosing,respectively.Schisandrae Fructus oil treatments also elevated the levels of serum TTP by 51%and63%,Apo B48 by 152%and 425%,and VLDL by 67%and 38%in mice,respectively.FSS and FSC oil treatments also increased liver mass by 53%and 55%and HGF by 106%and 174%,but lowered serum ALT activity by 38%and 22%,respectively.Fenofibrate pre/co-treatment attenuated the FSS and FSC oil-induced elevation in serum TG levels by 41%and 49%at 48 h post-dosing,respectively,but increased hepatic TG contents(by 38%and 33%,respectively)at 12 h post-dosing.Conclusions:Our findings provide evidence to support the establishment of a novel mouse model of hypertriglyceridemia by oral administration of FSS oil(mainly increasing endogenous TG)and FSC oil(mainly elevating exogenous TG).

Niaoduqing granules inhibits TGF-β1-induced epithelial-mesenchymal transition in human renal tubular epithelial HK-2 cells

Objective Chronic renal failure(CRF)is a worldwide public health burden.Niaoduqing granules(NDQ)is widely used for CRF treatment in China.However,the underlying mechanism of NDQ is not fully studied.This study is aimed to investigate whether NDQ ameliorate CRF by inhibiting transforming growth factor-β1(TGF-β1)-induced EMT in human renal tubular epithelial HK-2 cells.Methods 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenylterazolium bromide assay and colony formation assay were used to investigate the cytotoxicity of NDQ in HK-2 cells.Morphological changes of HK-2 cells after TGF-β1 or/and NDQ treatment were observed under a microscope.Wound-healing,migration and invasion assays were performed to determine the cell movement,migratory and invasive abilities,respectively.Western blot analysis was carried out to examine the protein levels of TGF-βreceptor I(TβRI)and epithelial-mesenchymal transition(EMT)-associated factors.Fluorescence confocal microscopy was applied to observe the organization of filamentous actin.Results NDQ suppressed TβRI expression dose-dependently.NDQ inhibited TGF-β1-stimulated EMT in HK-2 cells,supported by the evidences that NDQ prevented morphology change,attenuated cell migration and invasion,downregulated EMT factors and reorganized filamentous actin distribution in TGF-β1-stimulated HK-2 cells.Conclusions NDQ attenuates chronic renal failure which may be associated with inhibition of TβRI expression and EMT process.

Non-stationary Subdivision for Exponential Polynomials Reproduction

In this paper we develop a novel approach to construct non-stationary subdivision schemes with a tension control parameter which can reproduce functions in a finite-dimensional subspace of exponential polynomials. The construction process is mainly implemented by solving linear systems for primal and dual subdivision schemes respectively, which are based on different parameterizations. We give the theoretical basis for the existence, uniqueness, and refinement rules of schemes proposed in this paper. The convergence and smoothness of the schemes are analyzed as well. Moreover, conics reproducing schemes are analyzed based on our theory, and a new idea that the tensor parameter ωk of the schemes can be adjusted for conics generation is proposed.