Systematic review of external applications combined with three-step analgesic therapy in treating primary liver cancer pain / 中国中药杂志

To systemically evaluate the clinical efficacy and safety of traditional Chinese medicine( TCM) external application combined with three-step analgesic therapy in treating primary liver cancer pain. CNKI,Wanfang,CBM,VIP,Medline and Cochrane Library and manual retrieval were used to search for the clinical randomized controlled trials on TCM external applications combined with three-step analgesic therapy in treating primary liver cancer pain from database establishment to January,2018. The bias risk of RCTs was assessed by using the Cochrane system evaluator's Manual,and the extracted data were analyzed by using Review Manager 5. 3. Finally sixteen Chinese articles were enrolled,including one high quality article and 1 164 patients. Meta-analysis showed that TCM external applications combined with three-step analgesic therapy could alleviate the cancer pain( OR = 3. 44,95% CI[2. 49,4. 75],P <0. 000 01); prolong pain relief time( SMD = 3. 42,95%CI[1. 83,6. 40],Z = 3. 85,P = 0. 000 1); and improve the cartesian score of the patients( OR = 3. 42,95%CI[1. 83,6. 40],P = 0. 000 01). Descriptive analysis showed that the intervention may effectively shorten the onset time of pain relief,reduce VAS and NRS scores,reduce the dose of morphine,and reduce the number of bursts of pain. At present,the evidences have shown that the combination of TCM external applications combined with three-step analgesic therapy in treating primary liver cancer pain has superior clinical efficacy as compared with the three-step analgesic therapy alone. However,the clinical trials of existing small-sized randomized controlled trials have low quality of methodology and require a large sample of high quality clinical trials for further validation.

Lesions Caused by Intracerebral Injection of Aquaporin-4 Immunoglobulin G / 中山大学学报(医学科学版)

[Objective]To investigate the pathological damage caused by aquaporin-4 antibody extracted from patients with neuromyelitis optica spectrum disorders(NMOSD)and the influence of systemic immune status on the local disease focus.[Methods]The C57BL/6 mice were chose for establishing experimental autoimmune encephalomyelitis (EAE).During the peak at onset,serum-derived immunoglobulin G(IgG)from aquaporin-4(AQP4)IgG positive patients and healthy human complement(hC)were injected in the brain parenchyma(EAE+AQP4-IgG+hC group,n=5).The EAE induced mice injected with normal saline(EAE+NS group,n=5)and mice without EAE injected with AQP4-IgG and hC from healthy volunteers(AQP4-IgG + hC group,n=5)were served as control groups. The dramatic loss of AQP4,astrocyte glial fibrillary acidic protein(GFAP),oligodendrocyte myelin basic protein(MBP)and the infiltration of inflammatory cells(T lymphocytes,neutrophils and macrophages)were compared with each group by using immunoflu-orescence,in order to find abnormal changes.[Results]Intracerebral injection of AQP4-IgG together with hC can cause NMO-like lesions,including astrocyte injury,demyelination and inflammatory cell infiltration.However,EAE mice model with intracerebral injection of AQP4-IgG and hC represented more significant loss of AQP4 and GFAP(P=0.008 and P=0.016,respectively)compared with mice without EAE induced.The area of MBP loss was also increased,while there′s no statistical difference.No statistical difference was also found in the number of vessels infiltrated with CD3+T cell,neu-trophils and the area infiltrated with macrophage. Astrocyte proliferation existed in all groups,but no loss of AQP4, GFAP and MBP was found in EAE mice injected with NS.[Conclusion]Intracerebral injection of AQP4-IgG and hC can cause distinct pathological damage and the pathology can be promoted by immune system activated by EAE.Intracerebral injection of AQP4-IgG and hC can mimic the pathogenesis of NMOSD better in EAE mice model.

Effects of Shehuang Paste on hemodynamics, endotoxin, nitric oxide and endothelin-1 in patients with refractory cirrhotic ascites / 中国结合医学杂志

<p><b>OBJECTIVE</b>To explore the influence of Shehuang Paste (SHP) to the hemodynamics, endotoxin, nitric oxide (NO), and endothelin-1 (ET-1) in patients with refractory cirrhotic ascites.</p><p><b>METHODS</b>Fifty-nine cases of refractory cirrhotic ascites were randomly assigned to two groups, 32 cases in the treatment group and 27 cases in the control group. The basic treatment was the same for both groups, including liver protecting medicines, diuretics and supportive drugs, but SHP navel sticking was applied for the treatment group additionally once a day. A course of one month of treatment was applied and the general efficacy on ascites was observed by the end of the therapeutic course. Before and after the treatment, examinations by limulus lysate chromogenic test was conducted to measure plasma endotoxin content; colorimetry to measure plasma content of NO indirectly, radioimmunoassay to measure plasma ET-1 content; and color Doppler ultrasonography to measure the blood flow of portal vein and splenic vein. The relationship between the blood flow of portal vein and splenic vein and endotoxin, NO and ET-1 in the treatment group was analyzed as well.</p><p><b>RESULTS</b>The total effective rate on ascites was 84.4% in the treatment group, and 48. 1% in the control group, with significant difference shown between them (P<0.01). In the treatment group the blood flow of portal vein and splenic vein, contents of endotoxin, NO and ET-1 all got significantly reduced after treatment ( P<0.05 or P<0.01); while these indexes in the control group were not significantly changed ( P 0.05). Moreover, it was found that in the treatment group, the blood flow of portal vein and splenic vein had a positive correlation to the levels of NO, ET-1, and endotoxin, either before or after treatment.</p><p><b>CONCLUSION</b>Application of SHP navel sticking could clearly reduce the blood flow of portal vein and splenic vein, and lower the content of endotoxin, NO and ET-1. The blood flow of portal vein and splenic vein in the treatment group showed a positive correlation with the contents of endotoxin, NO and ET-1. liver cirrhosis, refractory ascites, vasoactive substance, hemodynamics</p>

Recombinant human interleukin-10 inhibits proliferation of vascular smooth muscle cells stimulated by advanced glycation end products and neointima hyperplasia after carotid injury in the rat / 生理学报

The purposes of this study was to determine the effects of recombinant human interleukin-10 (rhIL-10) on proliferation of vascular smooth muscle cells (VSMCs) stimulated by advanced glycation end products (AGE) and neointima hyperplasia after rat carotid arterial injury. Rat aortic VSMCs were cultured and treated with rhIL-10 or AGE respectively, and then co-treated with rhIL-10 and AGE. Proliferation of VSMCs was quantified by colormetric assay. Cell cycle analysis was performed by flow cytomertry. Sprague-Dawley rats were treated with recombinant human IL-10 (rhIL-10) for 3 d after carotid arteries injury. The ratio of neointima to media area at the site of arterial injury was measured 28 d after balloon injury. The p44/42 MAPK activity was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Compared to control, AGE stimulated VSMCs proliferation. rhIL-10 alone had no effect on VSMCs growth. With AGE stimulation, rhIL-10, at dose as low as 10 ng/ml, inhibited VSMCs growth (P<0.05). The cell number in G(0)/G(1) phase of AGE and rhIL-10 co-treatment group was higher than that of AGE treatment alone (P<0.01) by flow cytometry analysis. Compared with the control group of neointima hyperplasia in rats, the ratio of neointima to media area of recombinant human IL-10 group was reduced by 45% (P<0.01). The p44/42 MAPK activity was significantly enhanced by AGE. The AGE effects were opposed by rhIL-10. The anti-inflammatory cytokine rhIL-10 inhibits AGE-induced VSMCs proliferation. Recombinant human IL-10 also inhibited neointima hyperplasia after carotid artery injury in rats. The results suggest the possibility that recombinant human IL-10, as a potential therapeutic approach, prevents neointimal hyperplasia.

Recombinant human interleukin-10 inhibits vascular smooth muscle cell proliferation induced by TNF-alpha / 生理学报

Vessel injury provokes a release in proinflammatory cytokines that influence vascular smooth muscle cell (VSMC) proliferation. The purposes of this study was to determine the effects of recombinant human interleukin-10 (rhIL-10) on rat vascular smooth muscle cell proliferation and the activity of p44/p42 mitogen-activated protein kinase (MAPK) promoted by tumor necrosis factor-alpha (TNF-alpha). Rat aortic VSMCs were cultured and treated with rhIL-10 or TNF-alpha respectively, and then cotreated with rhIL-10 and TNF-alpha. The proliferation of VSMCs was quantified by colormetric assay. Cell cycle analysis was performed by flow cytometry. The p44/42 MAPK activity was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Compared to control group, TNF-alpha stimulated significantly VSMC proliferation in TNF-alpha group. rhIL-10 alone had no effect on VSMC growth, but significantly inhibited VSMC proliferation induced by TNF-alpha at a dose of 10 ng/ml. The cell number in G(0)/G(1) phase of TNF-alpha and rhIL-10 co-treatment group was higher than that of TNF- alpha group (P<0.01) by flow cytometry analysis. The p44/42 MAPK activity was significantly enhanced by TNF-alpha and the TNF-alpha effect was opposed by rhIL-10. It is suggested that rhIL-10 can inhibit TNF-alpha induced VSMC proliferation and phosphorylation of p44/42 MAPK.