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To observe the effect of curcumin treatment on serum inflammatory factors in rats with traumatic arthritis and explores the protective effect of articular surface cartilage in rats with traumatic arthritis. A control group (group A), a model group (group B), and a curcumin group (group C) were randomly chosen. Except for the group A, the curcumin model was established by removing the medial meniscus of the right knee in the other two groups. After the model was successfully established, the group C was intraperitoneally injected with curcumin solution 50 mg/kg, while the group A and B were injected with the same volume of dimethyl sulfoxide solution for 28 d. The levels of serum vascular endothelial growth factor and tumor necrosis factoralpha and interleukin-1 beta were measured by enzyme-linked immunosorbent assay method. The arthritis index score of the two groups was calculated, the pathological morphology of articular cartilage was observed by hematoxylin and eosin staining, and the apoptosis rate of knee chondrocytes was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Real-time polymerase chain reaction and Western blot methods were used to detect the expression of autophagy and apoptosis regulatory molecules Beclin-1, B-cell lymphoma 2, caspase-3, messenger ribonucleic acid and protein in knee cartilage. Curcumin can protect the articular surface cartilage of traumatic arthritis rats by reducing inflammatory factors in serum and regulating the apoptosis and autophagy of articular chondrocytes. Curcumin may be a potential drug for the treatment of traumatic arthritis. [ABSTRACT FROM AUTHOR]

The effect of recombinant human bone morphogenetic protein-2 mediated wingless-related integration site beta-catenin pathway on bone defect repair and angiogenesis of rabbit radius was explored. 18 New Zealand rabbits were divided into 3 groups, control group (group A), low dose recombinant human bone morphogenetic protein-2 group (group B), and high dose recombinant human bone morphogenetic protein-2 group (group C). The bone mineral density of each group was compared. Rabbit bone marrow mesenchymal stem cell line cells were resuscitated and the proliferation ability, protein expression, messenger ribonucleic acid expression and cell migration ability of the three groups were detected by cell counting kit-8, Western blot, quantitative polymerase chain reaction and Transwell methods. The radial bone mineral density of rabbits in the group B was higher than that in group A at 4 w and 8 w, while in group C was higher than that group B. The cell proliferation and migration activity in the group B increased than group A, while those in the group C were raised than the group B. The protein levels of angiopoietin-1 and vascular endothelial growth factor in group B increased than those in the group A and these levels in group C raised comparatively than in group B. The relative expression of wingless-related integration site beta and catenin in group B reduced than group A, while this expression in group C was lower than group B. Recombinant human bone morphogenetic protein-2 can promote the repair of radial bone defect and angiogenesis by mediating wingless-related integration betacatenin pathway in rabbits. [ABSTRACT FROM AUTHOR]

This study aims to examine the impact and underlying mechanism of micro ribonucleic acid-515-5p on the biological behavior of colorectal cancer cells. The study conducted an experiment categorizing into control (blank), colorectal cancer, and micro ribonucleic acid-515-5p overexpression groups. Western blot, quantitative polymerase chain reaction techniques, cell counting kit-8, and Transwell methods were used to detect the growth and metastasis ability of the cells, the expression level of the related protein and messenger ribonucleic acid. The micro ribonucleic acid-515-5p messenger ribonucleic acid was found to be significantly reduced in colorectal cancer group cells compared to control group cells. The proliferation activity and migration number of the cells in micro ribonucleic acid-515-5p overexpression group were reduced compared to the colorectal cancer group cells. The first apoptosis signal, B-cell lymphoma 2-associated X protein, and first apoptosis signal ligand in the micro ribonucleic acid-515-5p overexpression group were higher compared to the colorectal cancer group, while the expression level of B-cell lymphoma 2 was lower compared to the colorectal cancer group. Protein kinase B, phosphoinositide 3-kinase, messenger ribonucleic acid and protein in the micro ribonucleic acid-515-5p overexpression group were reduced than the colorectal cancer group. The overexpression of micro ribonucleic acid-515-5p has been observed to exert inhibitory effects on proliferation, migration, and invasion of colorectal cancer cells, while induce apoptosis of colorectal cancer cells by inhibiting phosphoinositide 3-kinase/protein kinase B signaling pathway. [ABSTRACT FROM AUTHOR]

To explore the activation effect and mechanism of exocrine secreted by HepG2.2.15 cells on hepatic stellate cells. The exosomes from HepG2.2.15 cell culture medium and HepG2 cell culture medium were co-cultured with hepatic stellate cells respectively. The activation of hepatic stellate cells after co-culture was detected by immunofluorescence, oil red staining, scratch test, transwell, EDU, cell counting kit-8, flow apoptosis and Western blotting. The microRNA and downstream pathways which may lead to the activation of hepatic stellate cells were extracted from HepG2.2.15 cell culture medium and HepG2 cell culture medium by exosome sequencing, which were verified by quantitative polymerase chain reaction and Western blotting. After coculture with hepatic stellate cells, exosomes secreted by HepG2.2.15 cells and exosomes secreted by HepG2 cells and hepatic stellate cells, the proliferation, migration and cell activity of hepatic stellate cells were enhanced. Quantitative polymerase chain reaction detection showed that the expression of microRNA1269a in exosomes secreted by HepG2.2.15 cells co-cultured with hepatic stellate cells and exosomes secreted by HepG2 cells increased compared with hepatic stellate cells co-cultured with hepatic stellate cells, while the expression of C-mesenchymal-epithelial transition factor in stromal epidermis decreased. The hepatic stellate cells of exosomes secreted by HepG2.2.15 cells co-cultured with hepatic stellate cells and exosomes secreted by HepG2 cells and hepatic stellate cells decreased while the Yes-associated protein increased compared with that of C-mesenchymal-epithelial transition factor and phosphorylated Yes-associated protein. The exocrine secreted by HepG2.2.15 cells promote the activation of hepatic stellate cells. The mechanism may be that the exocrine carrier microRNA-1269a secreted by HepG2.2.15 is down-regulated by hepatic stellate cells, which downregulates c-mesenchymal-epithelial transition factor messenger ribonucleic acid, resulting in the decrease of C-mesenchymal-epithelial transition factor receptors on the surface of hepatic stellate cells, resulting in the decrease of Yes-associated protein phosphorylation and promoting the proliferation and activation of hepatic stellate cells. [ABSTRACT FROM AUTHOR]

Previous literature has described the significant biological and pharmacological activities of rutin in mammals. Nevertheless, there is no known function or role for rutin in spinal cord neuroinflammation. In this research, 120 male adult Sprague-Dawley rats were randomly divided into 4 groups (n=30 per group) viz., sham operation (control group), spinal cord injury, methylprednisolone treatment and rutin treatment. Enzyme-linked immunosorbent assay analysis of pro-inflammatory cytokines, malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase were analyzed using kits. Fibroblast growth factor, neurotrophin 3, brain-derived neurotrophic factor, and nerve growth factor, messenger ribonucleic acid level were examined using real-time fluorescent quantitative polymerase chain reaction. Western blot analysis of p38 mitogen-activated protein kinase protein expression relative to the model group (spinal cord injury group), inflammatory cytokines, malondialdehyde levels, spinal cord water content, and p38 mitogen-activated protein kinase protein levels were reduced in the rutin treatment group, however, the superoxide dismutase, catalase, and glutathione peroxidase levels, fibroblast growth factor, neurotrophin 3, brain-derived neurotrophic factor, and nerve growth factor, messenger ribonucleic acid levels, and the blood-brain barrier score (24, 48, 72 h) were increased. Rutin relieves spinal cord neuroinflammation by inhibiting the p38 mitogen-activated protein kinase signaling pathway. [ABSTRACT FROM AUTHOR]

Cyclophilin A regulates the biological behavior of placental trophoblast cells in severe preeclampsia by regulating oxygen inducible factor (hypoxia-inducible factor-1 alpha) signal pathway. JEG3 cell line was selected and randomly divided into control group (minimum essential medium 1 l containing 10 % fetal bovine serum) (group A), low dose group (cyclophilin A protein concentration was 1 pg/ml) (group B) and high dose group (cyclophilin A protein concentration was 3 pg/ml) (group C). The apoptosis of JEG3 cells was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling method, the expression of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta messenger ribonucleic acid in JEG3 cells was detected by quantitative read-time polymerase chain reaction method, and the expression of cleaved caspase-3, caspase-3, cleaved poly (ADP-ribose) polymerase 1, poly (ADP-ribose) polymerase 1, p53 and hypoxia-inducible factor-1 alpha protein was detected by Western bolting. Quantitative polymerase chain reaction assay showed that the expression levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta in group B and group C were raised than those in group A, and the expression levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta increased with the increase of cyclophilin A concentration. Western blotting detection showed that the cleaved caspase-3 expression level of JEG3 cells in group B and C was raised than that in group A, and increased with the increase of concentration, while the expression of cleaved poly (ADP-ribose) polymerase 1 in group C was raised than that in group A. The levels of hypoxia-inducible factor-1 alpha in JEG3 cells were higher in both the group B and C compared to the group A, and they further increased with the rise in concentration. Cyclophilin A can promote inflammation by increasing the expression of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta in trophoblasts, and accelerate the apoptosis of trophoblasts by activating caspase-3 pathway, which is an important pathogenic factor of preeclampsia. This mechanism may be related to the regulation of hypoxia-inducible factor-1 alpha signal pathway. [ABSTRACT FROM AUTHOR]

The aim of this study is to examine the suppressive impact of astragaloside on the invasion and spread of non-small cell lung cancer by obstructing the transforming growth factor-beta/focal adhesion kinase/protein kinase B signaling pathway. Sixty mice were categorized into three groups; the normal control group (n=20) (group A), the model control group (n=20) (group B), and the astragaloside IV intervention group (n=20) (group C). To establish the non-small cell lung cancer mouse model for group B and group C, the modulated PC9/ER cell suspension was injected into the left axilla of nude mice, whereas group A received an equivalent amount of normal saline instead. After successful modeling, mice in group C were given astragaloside 30 mg/kg by intragastric administration. The expression levels of transforming growth factor-beta, focal adhesion kinase, and protein kinase B messenger ribonucleic acid were higher in group B compared to group A, whereas the expression levels of transforming growth factor-beta, focal adhesion kinase, and protein kinase B messenger ribonucleic acid were lower in group C compared to group B. The levels of protein expression for transforming growth factor-beta, focal adhesion kinase, and protein kinase B were higher in group B compared to group A, whereas the levels of protein expression for transforming growth factor-beta, focal adhesion kinase, and protein kinase B were lower in group C compared to group B. The non-small cell lung cancer is influenced by astragaloside A, transforming growth factor-beta, focal adhesion kinase, and protein kinase B. [ABSTRACT FROM AUTHOR]

To explore the renal protection mechanism of targeted regulating of transforming growth factor beta receptor type 1 expression by let-7a in diabetic nephropathy rats, diabetic nephropathy rats were created through high-sugar and high-fat diet combined with a small dose of streptozotocin. Normally reared rats were taken as control group. Diabetic nephropathy rats were divided into two groups, one group was treated with let-7a analogs group, and the other group was not treated (diabetic nephropathy group). Experimental results showed that diabetic nephropathy rats had symptoms such as increased dietary frequency, weight loss, proteinuria, and decreased creatinine clearance. After let-7a treatment, the proteinuria symptoms of rats in let-7a analogs group were notably improved, and the creatinine clearance rate increased. The expression level of collagen IV in let-7a analogs group was higher than that of the control, but the difference was not significant. The expression level of fibronectin increased significantly in the diabetic nephropathy group (p<0.05), and that of the let-7a analogs group was significantly lower than that of the diabetic nephropathy group (p<0.05). The immunofluorescence expression result was consistent with the expression trend detected by Western blot. Compared with the control, the expressions of transforming growth factor-beta 1, transforming growth factor beta receptor type 1, and mothers against decapentaplegic homolog 2 in the diabetic nephropathy group were evidently increased (p<0.05), and the expression of mothers against decapentaplegic homolog 7 decreased obviously (p<0.05). The protein expression level was consistent with the messenger ribonucleic acid expression result. In summary, by regulating the levels of collagen IV and fibronectin and targeting the transforming growth factor beta receptor type 1 pathway, let-7a inhibited extracellular matrix synthesis to protect kidney function in patients with diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Breast cancer is the cancer with the highest incidence in women in the world. It was to investigate the mechanism of chemotactic cytokine binding protein D6 in the tumorigenicity and metastasis of breast cancer cell. The more invasive human breast cancer cell lines MDA-MB-435 and MDA-MB-231, the less invasive human breast cancer cell lines ZR-75-30 and ZR-75-1, and normal breast epithelial cells Hs578Bst and human normal breast epithelial cell line- 100 were selected for the experiments. The differences of D6 messenger ribonucleic acid levels in different cells and the effects of other factors on D6 messenger ribonucleic acid levels were explored. Then, MDA-MB-435 was selected for D6 transfection to make over expressed MDA-MB-435/D6 cells, and the effect of D6 on the tumorigenicity and metastasis of MDA-MB-435 was analyzed by comparative analysis. It revealed as the increasing cell invasion, the D6 messenger ribonucleic acid was obviously decreased; as the increasing interleukin-1 beta concentration, the D6 messenger ribonucleic acid increased clearly; as the raising tumor necrosis factor alpha concentration, the D6 messenger ribonucleic acid was clearly decreased in different degrees (p<0.05). Interferon gamma concentration had no effect on D6 messenger ribonucleic acid level (p>0.05). As against MDA-MB-435 cells, the proliferation and migration of MDA-MB-435/D6 cells were clearly decreased from the 3rd d; the concentrations of C-C motif ligand 2, C-C motif ligand 4, and C-C motif ligand 13 of D6 ligands in MDA-MB-435/D6 were clearly lower (p<0.05). Chemotactic cytokine binding protein D6 is negative regulatory in breast cancer, inhibiting the tumorigenicity and metastasis of breast cancer cell. [ABSTRACT FROM AUTHOR]

To explore the effects and possible mechanisms of erlotinib combined with radiotherapy on the proliferation and apoptosis of human non-small cell lung cancer cells. Blank control group, non-small cell lung cancer group and erlotinib group were set cells in the blank control group were human bronchial epithelioid cells without any treatment and cultured routinely. The proliferation ability of the cells in the three groups was detected by cell counting kit-8, Western blot was used to assess protein expression, quantitative polymerase chain reaction was used to measure messenger ribonucleic acid expression, and Transwell was used to determine metastatic potential. The quantity of migrating cells and the rate of cell growth of non-small cell lung cancer group were higher than that of blank control group; the cell metastasis activity number of erlotinib group were reduced than that of non-small cell lung cancer group. The cell invasion number of non-small cell lung cancer group was higher than blank control group; erlotinib group was reduced than that of non-small cell lung cancer group. The overall apoptosis rate was higher than the non-small cell lung cancer group. The apoptotic proteins Fas, B-cell lymphoma 2-associated X protein and Fas ligand were higher in the erlotinib group than in the non-small cell lung cancer group, and the B-cell lymphoma 2 was reduced than the nonsmall cell lung cancer group. The 5' adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptor coactivator-1 alpha in the non-small cell lung cancer group were reduced than the blank control group and erlotinib group were higher than the non-small cell lung cancer group. The protein mitogen-activated protein kinase and peroxisome proliferator-activated receptor coactivator-1 alpha in the non-small cell lung cancer group were reduced than the blank control group and erlotinib group were higher than those in the non-small cell lung cancer group. The mechanism of erlotinib’s capacity to lower the viability of non-small cell lung cancer cells, block their proliferation, migration, and invasion ability, and induce apoptosis may be connected to the control of the 5' adenosine monophosphate-activated protein kinase/ peroxisome proliferator-activated receptor coactivator-1 alpha signaling pathway. [ABSTRACT FROM AUTHOR]

Psoriasis is a chronic immune-mediated inflammatory skin disease in which gamma delta T cells play an important role. Chinese herbal medicine Jia Wei Jing Xie Yin has its origin in Jing Xie Yin, a medicine created by the traditional Chinese medicine doctor Wu Jun. Previous studies have shown that Jia Wei Jing Xie Yin has good clinical efficacy for patients with blood-heat type psoriasis by inhibiting the interleukin-23/T-helper 17 immune inflammation axis. This study aims to determine the immunoregulatory effects and the underlying mechanisms of Jia Wei Jing Xie Yin in psoriasis-related inflammatory responses. Bagg albino mice with imiquimod-induced psoriasis-like dermatitis were treated with saline (Model), methotrexate that serves as a positive control, or low, medium and high doses of Jia Wei Jing Xie Yin intragastrically. The pathological changes, inflammatory cell infiltration, the expression of inflammatory cytokines, and Janus tyrosine kinase 3/signal transducers and activators of transcription pathwayrelated proteins in the skin lesion were examined. The abundance of Vγ4+ T cells in lymph nodes and spleen was determined by flow cytometry. Jia Wei Jing Xie Yin ameliorated psoriasis area and severity index scores, reduced the infiltration of inflammatory cells and interleukin-17 producing gamma delta T cells, inhibited the messenger ribonucleic acid expression of interleukin-17, interleukin-22, interleukin-6, tumour necrosis factor alpha and matrix metalloproteinase-9, reduced inflammatory cell infiltration and pathological damage. Nevertheless, the expression of the Janus tyrosine kinase 3/signal transducers and activators of transcription signaling pathway was not significantly changed in the MTX and Jia Wei Jing Xie Yin groups. Our work demonstrates that Chinese herbal medicine Jia Wei Jing Xie Yin alleviates Imiquimod-induced inflammation in psoriasis. We have found a good regulatory effect of Jia Wei Jing Xie Yin on gamma delta T cells. [ABSTRACT FROM AUTHOR]