OBJECTIVE: To observe the effect of high-dose Astragalus injection and cyclophosphamide (CTX) on infection, urine protein and immune function of the patients with lupus nephritis. METHODS: Forty-three patients diagnosed as systemic lupus erythematosus (SLE) complicated by kidney damage and qi-deficiency syndrome were randomly divided into trial group (n=23) and control group (n=20). Patients in both groups were treated for 3 months. Intravenous drip infusion of 0.8 g CTX was administered to all patients once a month, while intravenous drip infusion of 20 ml Astragalus injection was only administered to patients in the trial group every day for 12 days in each month. RESULTS: The decrease of active clinical symptom score after the treatment in the trial group was greater than that in the control group (P<0.05). The infection rates of the trial group and the control group were 4.35% and 25% respectively. The decrease of 24-hour urine protein and CD8, and the increase of red blood cell count and serum albumin in the trial group were greater than those in the control group, and there were significant differences between the two groups (P<0.05). White blood cell count in the trial group was decreased less than that in the control group after the treatment (P<0.05). CONCLUSION: High-dose Astragalus injection used together with CTX is more effective than CTX alone in decreasing infection rate and urine protein and improving immune function for patients with lupus nephritis.

Objective To observe the therapeutic effect of Ziyin Yangxue Qingre Formula (Formula for enriching yin,nourishing blood and clearing heat) on primary Sjogren's Syndrome (pSS).Methods Totally 64 female pSS patients were randomized into a treating group (33 cases),and a control group (31 cases).The control group was administered Hydroxychloroquine Sulfate Tablet.In addition,the treating group was prescribed Ziyin Yangxue Qingre Formula.Three-month treatment was as one course.After one course of treatment,the changes in symptom scores,salivation quantity,tear quantity,and immuno-infective indices were observed to compare the effect between both groups.Results The total effective rate of the treating group(87.88%) was significantly higher than that (64.52%) of the control group (P

Objective To expound the mechanism and the clinical features of Tong-Du-Huo-Luo exercise in treating ankylosing spondylitis.Methods Besides taking SASP per os,the patients in treatment group did Tong-Du-Huo-Luo exercise twice daily. Patients in control group took SASP only.The patients in both groups had accepted the treatments for 6 months.Results Compared with western medicine treatment,the Tong-Du-Huo-Luo exercise can bring better effects on ability of expanding chest,finger-floor distance,pulvinar-wall distance,and improving the results of Schober test and blood sedimentation test.Conclusions Tong-Du-Huo-Luo exercise is an effective method in treating ankylosing spondylitis patients.

Objective To study the effect of 1?,25-dihydroxyvitamin D3[1,25-(OH)2D3] on cytoskeleton,gap junction intercellular communication (GJIC) and intracellular Ca2+ ([Ca2+]i) in osteoblasts (OB) in vitro. Method OB were isolated from calvaria bone. After 20 min and after 24 h treated by 1,25-(OH)2 VD3 (0,10-9,10-8,10-7 mol/L),[Ca2+]i was evaluated. F-actin and GJIC were observed after 24 and 48 h incubation later. Results Compared with the control group,[Ca2+]i in all 1,25-(OH)2 D3 groups was increased significantly at 20 min. [Ca2+]i in 10-9 mol/L 1,25-(OH)2D3 group was the lowest at 24 h after treatment. OB in 10-8 and 10-7 mol/L 1,25-(OH)2D3 groups were flat,and stress fibers were formed. The expression of F-actin in control group and 10-9 mol/L 1,25-(OH)2D3 group was reduced at 48 h after treatment. Compared with the control group,GJIC was weakened very significantly after treated with 10-9 mol/L 1,25-(OH)2D3 at 48 h,but enhanced very significantly in the group with 10-8 and 10-7 mol/L. Conclusion Higher dosage of 1,25-(OH)2D3 can maintain the morphology of OB and stimulate the communication among OB,but lower dosage can inhibit it.

The purpose of this study was to determine whether the Ca2+ signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-kappaB ligand (RANKL) to stimulate osteoclastogenesis and then treated with different concentrations of OPG, an inhibitor of osteoclast differentiation. The intracellular Ca2+ concentration [Ca2+]i and phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the different treatment groups were measured by flow cytometry and Western blotting, respectively. The results confirmed that M-CSF + RANKL significantly increased [Ca2+]i and CaMKII phosphorylation in osteoclasts (p < 0.01), and that these effects were subsequently decreased by OPG treatment. Exposure to specific inhibitors of the Ca2+ signaling pathway revealed that these changes varied between the different OPG treatment groups. Findings from the present study indicated that the Ca2+ signaling pathway is involved in both the regulation of osteoclastogenesis as well as inhibition of osteoclast differentiation and activation by OPG.
Animals ; Calcium/*metabolism ; *Calcium Signaling ; *Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Gene Expression Regulation/drug effects ; Macrophage Colony-Stimulating Factor/metabolism ; Mice ; Osteoclasts/*cytology/*drug effects/*metabolism ; Osteoprotegerin/*pharmacology ; RANK Ligand/metabolism

Objective To investigate the clinical efficacy of capecitabine metronomic chemotherapy in the maintenance of elderly patients with metastatic breast cancer. Methods Fifty-six patients with metastatic breast cancer treated in Jiangsu Shengze Hospital from April 2014 to April 2017 were randomly divided into two groups according to random number table method: metronomic chemotherapy group (n = 28) and conventional chemotherapy group (n = 28). The patients in the metronomic chemotherapy group were treated with capecitabine 500 mg, 2 times/d and continuous oral administration. The conventional chemotherapy group received capecitabine 1 250 mg, 2 times/d for 14 days, rested for 7 days, 21 days was a course of treatment.After two courses,the clinical efficacy,toxicity and quality of life were evaluated. Results There were no significant differences in RR and DCR between the metronomic chemotherapy group and conventional chemotherapy group (RR: 39.3 % vs. 42.8 %, DCR: 89.3 % vs. 85.7 %, both P > 0.05). The median progression-free survival (PFS) time in the metronomic chemotherapy group was 5.8 months (95 % CI 3.23-7.44, P= 0.764) and median overall survival (OS) time was 7.9 months (95 % CI 4.15-7.95, P=0.519). The median PFS time in the conventional chemotherapy group was 7.2 months (95 % CI 3.32-6.33, P=0.835), median OS time was 10.3 months (95 % CI 4.08-7.37, P=0.463). There was no significant difference between the two groups (both P> 0.05). The incidences of hand-foot syndrome, myelosuppression and digestive tract reaction in conventional chemotherapy group were higher than those in metronomic chemotherapy group, there were significant differences between the two groups (all P < 0.05). No Ⅲ-Ⅳ level adverse reactions were found in the metronomic chemotherapy group. The overall rate of improvement of the quality of life in the metronomic chemotherapy group was significantly higher than that in the conventional chemotherapy group (92.9 % vs. 78.8 %, χ 2= 7.629, P < 0.05). Conclusion The clinical efficacy of capecitabine metronomic chemotherapy in the maintenance of elderly patients with metastatic breast cancer is similar to conventional dose maintenance therapy,but it can not only reduce the side effects, but also improve the quality of life of patients.

Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In this study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells. Mechanistically, we found that Cd exposure decreased expression of connexin 43 (Cx43), increased expression of p-Cx43 and elevated intracellular free Ca2+ concentration, corresponding to a decrease in gap junctional intercellular communication. Gap junction blockage pretreatment with 18β-glycyrrhizic acid (GA) promoted Cd-induced apoptosis, involving changes in expression of Bax, Bcl-2, caspase-3 and the mitochondrial transmembrane electrical potential (Δψm). Additionally, GA was found to enhance ERK and p38 activation during Cd-induced activation of mitogen-activated protein kinases, but had no significant effect on JNK activation. Our results indicated the apoptosis-related proteins and the ERK and p38 signaling pathways may participate in gap junction blockage promoting Cd-induced apoptosis in BRL 3A cells.
Animals ; Apoptosis/*drug effects ; Cadmium/*toxicity ; Calcium/metabolism ; Cell Communication/drug effects ; Connexin 43/genetics ; Enzyme Activation/drug effects ; Gap Junctions/*drug effects ; Gene Expression Regulation/drug effects ; Hepatocytes/cytology/*drug effects ; Rats ; Signal Transduction/drug effects

Exposure to cadmium (Cd) induces apoptosis in osteoblasts (OBs); however, little information is available regarding the specific mechanisms of Cd-induced primary rat OB apoptosis. In this study, Cd reduced cell viability, damaged cell membranes and induced apoptosis in OBs. We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increased concentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment. Cd also increased the phosphorylation of p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (JNK) in OBs. Pretreatment with the caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, ERK1/2 inhibitor (U0126), p38 inhibitor (SB203580) and JNK inhibitor (SP600125) abrogated Cd-induced cell apoptosis. Furthermore, Cd-treated OBs exhibited signs of oxidative stress protection, including increased antioxidant enzymes superoxide dismutase and glutathione reductase levels and decreased formation of reactive oxygen species. Taken together, the results of our study clarified that Cd has direct cytotoxic effects on OBs, which are mediated by caspase- and MAPK pathways in Cd-induced apoptosis of OBs.
Animals ; Apoptosis/*drug effects ; Cadmium/*toxicity ; Caspases/metabolism ; Environmental Pollutants/*toxicity ; Osteoblasts/*drug effects/metabolism ; Oxidative Stress/drug effects ; Rats ; Rats, Sprague-Dawley ; p38 Mitogen-Activated Protein Kinases/metabolism