To investigate whether chemically modified non-anticoagulation heparin derivate (periodate oxidation/borohydride reduction-modified heparin (OR-heparin)) could inhibit high glucose-induced human mesangial cell apoptosis and to explore its possible mechanism.Methods:Mesangial cells were exposed to high glucose or high glucose with OR-heparin for 24 h.Apoptosis was evaluated by Hoechst 33258 staining and Fluorescent activated cell sorting analysis.The expressions of apoptosis-related proteins ( p53,Bcl-2,Bax,cytosolic cytochrome C) were determined by Western blotting.NF-kB translocation was observed under fluorescence microscopy by using Cy3-1abeled antibody.Caspase-3 activity was detected by colorimetry.Results:OR-heparin significantly inhibited high glucose-induced mesangial cell apoptosis and the expression of apoptosis-related proteins.It also blocked NF-kB translocation induced by high glucose.Conclusion:OR-heparin inhibits high glucose-induced mesangial cell apoptosis through inhibiting the expression of apoptosis-related proteins and it may be due to the blockage of the translocation of NF-kB.

Natural polysaccharides are a kind of hydrophilic polymers.By grafting hydrophobic moieties to the polysaccharide backbone,could form self-assembled micelle with core-shell structure in aqueous by undergoing intramolecular or intermolecular association between hydrophobic moieties.The self-assembly micelles of amphiphilic polysaccharides provides a positive outlook for drug delivery systems with biodegradability,low antigenicity,good biocompatibility and so on.This review focus on biological activity of amphiphilic polysaccharide as self-assembly carriers,the principle of self-assembly of polymeric micelles,and the recent progress in hydrophobic modification of natural polysaccharides.

ObjectiveTo investigate the synergistic effect of Coptidis Rhizoma crude polysaccharide （CCP） and berberine （BBR） in treating ulcerative colitis （UC） model mice. MethodThirty male BALB/c mice were randomized into five groups. Except the 6 mice in the normal group， the rest were given 5% dextran sodium sulfate in their daily drinking water to establish the UC model. After modeling， the mice were administrated with corresponding agents by gavage once daily for 4 days： BBR （100 mg·kg^-1） group， BBR （100 mg·kg^-1） + low-dose （22.8 mg·kg^-1） CCP group， BBR （100 mg·kg^-1） + high-dose （45.6 mg·kg^-1） CCP group. The mice in the model group and normal group were administrated with the same volume of normal saline. At the end of the experiment， the mice were sacrificed for the collection of colon， and the expression of tight junction proteins zonula occluden-1 （ZO-1）， Claudin-1， and Occludin in colon tissue was detected by Western blot. With the normal group as the control， the disease activity index （DAI） score， colon length， colon histomorphology， and expression levels of tight junction proteins in other groups were evaluated. ResultCompared with the normal group， the modeling down-regulated the protein levels of ZO-1， Claudin-1， and Occludin （P<0.01）. Compared with the model group， BBR did not significantly change the protein level of Claudin-1 and up-regulated those of ZO-1 and occludin （P<0.01）. The expression levels of Claudin-1， ZO-1， and Occludin were up-regulated in BBR + CCP groups （P<0.01）. The expression levels of tight junction proteins in BBR + CCP groups were significantly higher than those in the BBR group （P<0.05）. ConclusionThe administration of CCP combined with BBR can effectively ameliorate intestinal mucosal barrier damage in the mice with UC.

Platycodon grandiflorus polysaccharide (PGP) is one of the main components of P. grandiflorus, but the mechanism of its anti-inflammatory effect has not been fully elucidated. The aim of this study was to evaluate the therapeutic effect of PGP on mice with dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) and explore the underlying mechanisms. The results showed that PGP treatment inhibited the weight loss of DSS-induced UC mice, increased colon length, and reduced DAI, spleen index, and pathological damage within the colon. PGP also reduced the levels of pro-inflammatory cytokines and inhibited the enhancement of oxidative stress and MPO activity. Meanwhile, PGP restored the levels of Th1, Th2, Th17, and Treg cell-related cytokines and transcription factors in the colon to regulate colonic immunity. Further studies revealed that PGP regulated the balance of colonic immune cells through mesenteric lymphatic circulation. Taken together, PGP exerts anti-inflammatory and anti-oxidant effect and regulates colonic immunity to attenuate DSS-induced UC through mesenteric lymphatic circulation.
Animals ; Mice ; Colitis, Ulcerative/drug therapy* ; Platycodon ; Colon/pathology* ; Cytokines ; Anti-Inflammatory Agents/therapeutic use* ; Polysaccharides/therapeutic use* ; Dextran Sulfate ; Disease Models, Animal ; Colitis/chemically induced* ; Mice, Inbred C57BL