[Curative effect of the combined therapy of warm acupuncture at back-shu points of five zang organs and western medicine on depression of yang deficiency pattern and its attenuating effect].

OBJECTIVE: To compare the therapeutic results and the occurrence of adverse reactions of medicine between the combined therapy of warm acupuncture at back-shu points of five zang organs and the western medicine and the simple wes-tern medication, and observe the therapeutic effect and attenuating effect of this combined therapy in treatment on depression of yang deficiency pattern. METHODS: A total of 80 patients with depression of yang deficiency pattern were randomly divided into an observation group and a control group （39 cases/group）. In the control group, escitalopram oxalate tablets were administered orally every day. In the observation group, on the base of the medication as the control group, warm acupuncture therapy was exerted at back-shu points of five zang organs, for 30 min each time, 5 times a week. The duration of treatment was 6 weeks in two groups. Before and after treatment, the scores of Hamilton depression scale (HAMD) and the antidepressant side effect scale (SERS) were evaluated and electroencephalogram (EEG) was detected; and the curative effect was assessed according to HAMD reduction rate in patients of the two groups. RESULTS: After treatment, the HAMD and SERS scores were lower than those before treatment in both groups. Compared with the control group, the HAMD and SERS scores were lower (P<0.05, P<0.01), and the EEG result was improved (P<0.01) in the observation group. The clinical total effective rate of the observation group was 97.43% (38/39), higher than 92.30% (36/39) of the control group (P<0.05). CONCLUSION: The combined therapy of warm acupuncture at back-shu points of five zang organs and western medicine effectively relieves depression of yang deficiency pattern in the patients and its overall therapeutic effect is better than simple western medication, besides, the combined therapy alleviates the adverse reactions induced by simple western medication.

Design and synthesis of 7-O-1,2,3-triazole hesperetin derivatives to relieve inflammation of acute liver injury in mice.

Based on the previous research results of our research group, to further improve the anti-inflammatory activity of hesperetin, we substituted triazole at the 7-OH branch of hesperetin. We also evaluated the anti-inflammatory activity of 39 new hesperetin derivatives. All compounds showed inhibitory effects on nitric oxide (NO) and inflammatory factors in lipopolysaccharide-induced RAW264.7 cells. Compound d5 showed a strong inhibitory effect on NO (half maximal inhibitory concentration = 2.34 ± 0.7 µM) and tumor necrosis factor-α, interleukin (IL)-1ß, and (IL-6). Structure-activity relationships indicate that 7-O-triazole is buried in a medium-sized hydrophobic cavity that binds to the receptor. Compound d5 can also reduce the reactive oxygen species production and significantly inhibit the expression of inducible NO synthase and cyclooxygenase-2 through the nuclear factor-κB signaling pathway. In vivo results indicate that d5 can reduce liver inflammation in mice with acute liver injury (ALI) induced by CCI4. In conclusion, d5 may be a candidate drug for treating inflammation associated with ALI.

PLK1 regulates hepatic stellate cell activation and liver fibrosis through Wnt/ß-catenin signalling pathway.

As an outcome of chronic liver disease, liver fibrosis involves the activation of hepatic stellate cells (HSCs) caused by a variety of chronic liver injuries. It is important to explore approaches to inhibit the activation and proliferation of HSCs for the treatment of liver fibrosis. PLK1 is overexpressed in many human tumour cells and has become a popular drug target in tumour therapy. Therefore, further study of the function of PLK1 in the cell cycle is valid. In the present study, we found that PLK1 expression was elevated in primary HSCs isolated from CCl4 -induced liver fibrosis mice and LX-2 cells stimulated with TGF-ß1. Knockdown of PLK1 inhibited α-SMA and Col1α1 expression and reduced the activation of HSCs in CCl4 -induced liver fibrosis mice and LX-2 cells stimulated with TGF-ß1. We further showed that inhibiting the expression of PLK1 reduced the proliferation of HSCs and promoted HSCs apoptosis in vivo and in vitro. Furthermore, we found that the Wnt/ß-catenin signalling pathway may be essential for PLK1-mediated HSCs activation. Together, blocking PLK1 effectively suppressed liver fibrosis by inhibiting HSC activation, which may provide a new treatment strategy for liver fibrosis.

Dexmedetomidine inhibits the invasion, migration, and inflammation of rheumatoid arthritis fibroblast-like synoviocytes by reducing the expression of NLRC5.

Rheumatoid arthritis (RA) is a chronic, autoimmune disease characterized by inflammatory synovitis, but its pathogenesis remains unclear. NLRC5 is a newly discovered member of the NLR family that is effective in regulating autoimmunity, inflammatory responses, and cell death processes. Dexmedetomidine (DEX) has been reported to have a variety of pharmacological effects, including anti-inflammatory and analgesic effects. However, the role of DEX in RA has not been explored. In adjuvant-induced arthritis (AA) rat models, DEX (10 µg/kg and 20 µg/kg) reduced the pathological score, the arthritis score, paw swelling volume, and the serum levels of IL-1ß, IL-6, IL-17A, and TNF-α. Moreover, by using Western blot and real-time quantitative PCR (RT-qPCR), it was demonstrated that DEX can inhibit the expression of IL-1ß, IL-6, MMP-3, MMP-9 and P-P65 in the synovial tissue of AA rats. In human rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs), DEX (250 nM and 500 nM) was found to inhibit the expression of IL-1ß, IL-6, MMP-3, MMP-9, and P-P65 following stimulation with TNF-α. Moreover, DEX can inhibit the invasion and migration of RA-FLSs stimulated by TNF-α. Finally, the expression of NLRC5 in RA-FLSs and AA rat models was also reduced by DEX. After silencing NLRC5 in RA-FLSs, the expression of IL-1ß, IL-6, MMP-3, MMP-9, and P-P65, as well as the invasion and migration of cells, were significantly reduced. These results indicate that DEX inhibits the invasion, migration, and inflammation of RA-FLSs by reducing the expression of NLRC5 and inhibiting the NF-κB activation.