Jianpi Qingchang decoction alleviates ulcerative colitis by inhibiting nuclear factor-κB activation

To investigate the therapeutic effect of Jianpi Qingchang decoction (JPQCD) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice.METHODSC57BL/c mice were injected intragastrically with 5% DSS instead of drinking water for 7 d, and their body weight, diarrhea severity and fecal bleeding were monitored, while the mice in the control group were treated with standard drinking water, without DSS. After 7 d, the DSS drinking water was changed to normal water and the DSS group continued with DSS water. The control and DSS groups were given normal saline by intragastric injection. The 5-aminosalicylic acid (5-ASA) group was treated orally with 5-ASA at a dose of 100 mg/kg daily. The JPQCD group was treated orally with JPQCD at a dose of 17.1 g/kg daily. On day 14, the colon length was measured, the colorectal histopathological damage score was assessed, and protein levels of interleukin (IL)-1β, IL-8 and tumor necrosis factor-alpha (TNF-α) in colon supernatants were measured by enzyme-linked immunosorbent assay. mRNA expression of IL-1β, IL-8, TNF-α and nuclear factor-kappa B (NF-κB) was detected by real-time quantitative polymerase chain reaction. Western blotting was used to detect the protein expression of NF-κB and inhibitor of kappa B.RESULTSAcute inflammation occurred in the mice administered DSS, including the symptoms of losing body weight, loose feces/watery diarrhea and presence of fecal blood; all these symptoms worsened at 7 d. The colons of mice treated with DSS were assessed by histological examination, and the results confirmed that acute inflammation had occurred, as evidenced by loss of colonic mucosa and chronic inflammatory cell infiltration, and these features extended into the deeper layer of the colon walls. The expression levels of IL-1β, IL-8 and TNF-α in the DSS group were higher than those in the control group (P < 0.05), and the expression levels of IL-1β, IL-8 and TNF-α in the JPQCD and 5-ASA groups were lower than those in the DSS group after treating with JPQCD and 5-ASA. Comparing with the DSS group, the mRNA level of IL-1β, IL-8, TNF-α and NF-κB was significantly reduced by 5-ASA and JPQCD. The difference between JPQCD and 5-ASA groups was not statistically significant (P > 0.05). Comparing with the DSS group, due to using JPQCD and 5-ASA, significant suppression of activation in DSS-induced NF-κB and increased phosphorylation of IκB in mice with experimental colitis occurred (P < 0.05). The difference between the JPQCD group and the 5-ASA group was not statistically significant (P > 0.05).CONCLUSIONActivation of the NF-κB signaling pathway is inhibited by JPQCD, which shows the potential mechanism by which JPQCD treats UC.

Jianpi Qingchang decoction regulates intestinal motility of dextran sulfate sodium-induced colitis through reducing autophagy of interstitial cells of Cajal

AIM To investigate the underlying effect of Jianpi Qingchang decoction(JQD) regulating intestinal motility of dextran sulfate sodium(DSS)-induced colitis in mice. METHODS C57BL/6 mice were randomly divided into four groups: the control group, the DSS group, the JQD group, and the 5-aminosalicylic acid group. Except for the control group, colitis was induced in other groups by giving distilled water containing 5% DSS. Seven days after modeling, the mice were administered corresponding drugs intragastrically. The mice were sacrificed on the 15^(th) day. The disease activity index, macroscopic and histopathologic lesions, and ultrastructure of colon interstitial cells of Cajal(ICC) were observed. The levels of tumor necrosis factor-alpha(TNF-α), interleukin(IL)-1β, IL-10 and interferon gamma(IFN-γ), the expression of nuclear factor-kappa B(NF-κB) p65, c-kit, microtubule-associated protein 1 light chain 3(LC3-Ⅱ) and Beclin-l m RNA, and the colonic smooth muscle tension were assessed. RESULTS Acute inflammation occurred in the mice administered DSS. Compared with the control group, the levels of IL-1β, TNF-α, IL-10 and IFN-γ, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency increased(P < 0.05), the expression of c-kit m RNA and the colonic smooth muscle contractile amplitude decreased in the DSS group(P < 0.05). Compared with the DSS group, the levels of IL-10 and IFN-γ, the expression of c-kit m RNA, and the colonic smooth muscle contractile amplitude increased(P < 0.05), the levels of TNF-α and IL-1β, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency decreased in the JQD group(P < 0.05).CONCLUSION JQD can regulate the intestinal motility of DSS-induced colitis in mice through suppressing intestinal inflammatory cascade reaction, reducing autophagy of ICC, and regulating the network path of ICC/smooth muscle cells.

Hydrothermal synthesis and electrochemical sensing properties of copper vanadate nanocrystals with controlled morphologies

Morphology-controlled synthesis of copper vanadate nanocrystals is of great significance in electrochemical sensing applications.A facile hydrothermal process for synthesizing copper vanadate nanocrystals with various morphologies(e.g.,nanoparticles,nanobelts and nanoflowers)was reported.Phase,morphology and electrochemical performance of the as-synthesized copper vanadate nanocrystals were characterized by X-ray diffraction(XRD),scanning electron microscope(SEM)and cyclic-voltammogram(CV)techniques.The results revealed that the morphologies of the Cu3V2O7(OH)2·2H2O(CVOH)nanocrystals could be controlled by changing copper salts,surfactants and pH values.The CVOH samples showed enhanced electrochemical response to ascorbic acid.Comparatively,the CVOH nanobelts had the higher electrochemical sensing performance than those of CVOH nanoparticles and nanoflowers.The CVOH-nanobelts-modified GCEs had a linear relationship between the peak currents in their CVs and ascorbic acid concentration.The CVOH nanocrystals can be used as potential electrochemical active materials for the determination of ascorbic acid.

Jianpi Qingchang Decoction-containing serum regulates the autophagy ofinterstitial cells

Objective： To investigate the effects of Jianpi Qingchang Decoction-containing serum （JQD-CS） on interstitial cells ofCajal （ICCs） autophagy and cell cycle arrest in vitro. Methods： ICCs were collected from the small intestines of miceand analyzed using an anti-c-Kit antibody. ICCs were divided into five groups： the blank group, the rapamycin group （anautophagy inducer）, the 5% （rapamycin ＋ 5% JQD-CS）, the 20% （rapamycin ＋ 20% JQD-CS） JQD-CS groups, and the3-Methyladenine （3-MA） group （rapamycin ＋ 3-MA; positive control）. Transmission electron microscopy was used toobserve the ultrastructure of ICCs. Western blotting was used to detect the expression of microtubule-associated protein1 light chain 3 （LC3-II）, Beclin-1, phosphatidylinositol 3-kinase （PI3K）, p-PI3K, protein kinase B （AKt）, p-AKt,mammalian target of rapamycin （mTOR）, and p-mTOR. Ca2＋ current was examined by patch-clamp experiments. Cellcycle was detected by flow cytometry. Results： Unlike in the rapamycin group, the ICC structures were more integratedand a lower number of autophagic vacuoles were observed in the 20% JQD-CS group. Moreover, the expression ofLC3-II and Beclin-1 decreased, the expression of c-Kit, p-PI3K, p-AKt increased, the maximum current density valuedecreased, and the number of cells in the G1 phase increased while those in the G2/M phase decreased, with the additionof 20% JQD-CS. Conclusion： JQD-CS can antagonize rapamycin-induced autophagy in ICCs in vitro by promoting thephosphorylation of PI3K/AKt pathway, inhibiting Ca2 ＋ inflow, and regulating the cell cycle.