Objective To explore the mechanism of flavonoids from scindapsus aureus in the treatment of DPN mice via NF-кB pathway. Methods A total of 60 mice were divided into 6 groups as follows, the control group, the model group, the low-dose, medium-dose and high-dose flavonoid groups, and the acarbose group, 10 cases per group. Schwann cells were divided into 5 groups: the normal group, the LPS group, and the low-dose, medium-dose and high-dose flavonoid groups. The nerve conduction function indexes, thermal pain threshold, levels of inflammatory factors, expression levels of NF-кB signaling pathway key proteins and their related mRNA were compared among different groups. Results Flavonoids from scindapsus aureus could increase the MNCV, the SNCV and the thermal pain threshold in mice, and reduce the levels of inflammatory factors (P< 0. 05). The flavonoid could decrease the ratios of p-NF-кB P65 / NF-кB P65 and p-IKKβ / IKKβ, and increase the p-IкBα / IκBα ratio (P< 0. 05). It could also down-regulate the expression levels of NF-кB P65 and IKKβ mRNA, and up-regulate the expression level of IкBα mRNA (P < 0. 05). Conclusion Flavonoids from scindapsus aureus can reduce the levels of inflammatory factors and relieve the symptoms in the DPN mice by inhibiting NF-κB signaling pathway. 

Objective To investigate the effect of artesunate (Art) on osteogenic differentiation of dental pulp stem cells (DPSCs) via AMPK/ NF-κB signaling pathway. Methods DPSCs were isolated and identified, the osteogenic and adipogenic differentiation of DPSCs were induced to evaluate the multi-lineage differentiation potential of the cells. DPSCs were treated with different concentrations of Art, and the cell proliferation activity was measured by the CCK-8 method. DPSCs were grouped into 4 groups as follows: the control group, the low-concentration artesunate group (Art-L), the medium-concentration artesunate group (Art-M), and the high-concentration artesunate group (Art-H). Alkaline phosphatase (ALP) staining was performed to measure the ALP activity in cells, and alizarin red S staining were performed to detect the cell mineralization nodules. Western blotting assay was performed to detect the expression levels of osteopontin (OPN), Runt-related transcription factor 2 (RUNX2), osteocalcin (OCN) and AMPK/ NF-κB pathway related proteins. Results In this study, DPSCs were successfully isolated and their multidirectional differentiation potential were verified. The ALP activity, the number of mineralized nodules, the protein expression levels of OPN, RUNX2, OCN, and p-AMPK were significantly increased in DPSCs treated with Art compared with the control group (P< 0. 05), while the expression level of p-NF-κB P65 protein was significantly decreased (P< 0. 05). Conclusion Art can promote the osteogenic differentiation of dental pulp stem cells, which may be related to the regulation of AMPK/ NF-κB signaling pathway. 

Objective To investigate the effect of lncRNA SNHG17 on the growth and metastasis of human chorionic trophoblast cells and its possible mechanism. Methods The expression levels of lncRNA SNHG17 and miR-525-5p in normal placental tissues and preeclampsia placental tissues were detected by qRT-PCR. Human chorionic trophoblast cells HTR-8 / SVneo were culturedin vitroand were transfected with the si-SNHG17, anti-miR-525-5p and their negative controls, respectively. The plate colony formation assay, scratch assay and transwell assay were used to detect the cell proliferation, migration and invasion, respectively. Dual-luciferase reporter assay was used to verify the targeting relationship between miR-525-5p and SNHG17. Results Compared with the normal placenta tissues, the expression level of lncRNA SNHG17 in preeclampsia placenta tissues was increased, while the expression level of miR-525-5p was decreased (P< 0. 05). After transfection with si-SNHG17, the number of colonies and invasive cells were increased, the wound healing rate was increased (P< 0. 05). lncRNA SNHG17 could bind with miR-525-5p. After the co-transfection of si-SNHG17 and anti-miR-525-5p, the number of colonies and invasive cells were decreased, the wound healing rate was decreased ( P < 0. 05 ). Conclusion Silencing lncRNA SNHG17 could promote the proliferation, migration and invasion of human chorionic trophoblast cells by upregulation of miR-525-5p.

Objective To explore the effect of CD168 on the proliferation and invasion of oral squamous cell carcinoma and its underlying mechanism. Methods The expression level of CD168 in the human normal oral keratinocyte cell line HOK and several oral squamous cell carcinoma cell lines was compared, and HN13 cell line was selected for the follow-up researches. Gene and protein expression levels of CD168 in cells infected with CD168 shRNA lentivirus were detected by using RT-qPCR and Western blotting. CCK-8 method was applied for the assay of the cell proliferation, the flow cytometry was used for the assay of cell apoptosis and the transwell assay was adopted to detect the cell invasion. Western blotting was performed to detect the expression levels of proteins related to cell proliferation, apoptosis, invasion and CXCL12-CXCR4 / CXCR7 signaling axis. Results The HN13 control cell line and the CD168-shRNA2 cell line were used for further studies (P < 0. 05). Silencing CD168 could suppress the proliferation and invasion of HN13 cells and increase its apoptosis rate (P< 0. 05). The protein expression levels of VEGF, PCNA, MMP-2, MMP-9, CXCL12, CXCR4 and CXCR7 were decreased in the shCH168 cells (P< 0. 05), while the Bax / Bcl-2 ratio was increased ( P < 0. 05), with no statistical changes observed between the shRNA-NC group and the control group (P > 0. 05). Conclusion Silencing of CD168 can inhibit the proliferation and invasion of oral squamous cell carcinoma cell line HN13, and promote their apoptosis, the mechanism may be related to the CXCL12-CXCR4 / CXCR7 signaling axis. 

Objective To investigate the effect of circular RNA (circRNA) circ_ 0061140 on the proliferation, cell cycle and apoptosis of non-small cell lung cancer cells via targeting miR-6838- 5p. Methods Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of circ_ 0061140 and miR-6838-5p in the non-small cell lung cancer cells. The NCI-H1299 non-small cell lung cancer cells were divided into 7 groups: the si-circ _ 0061140 group (transfected with si-circ_ 0061140, circ_ 0061140 lowly expressed), the si-NC group (transfected with si-NC, the negative control), the NC group (blank control with no transfection of miRNA), the miR-6838-5p group ( transfected with miR-6838-5p mimic, miR-6838-5p highly expressed), the miR-NC group ( transfected with miR-NC, the negative control), the si-circ_ 0061140 + anti-miR-NC group (co-transfected with si-circ_ 0061140 and anti-miR-NC), the si-circ_ 0061140 + anti-miR-6838-5p group ( co-transfected with si-circ_ 0061140 and anti-miR-6838-5p). Western blotting was used to detect the expression levels of cyclin D1 and cleaved cysteinyl aspartate specific proteinase-3 ( cleaved-caspase-3). The proliferation of cells was detected by MTT method. The cell cycle and cell apoptosis was detected by the flow cytometry. Dual luciferase reporter assay was used to verify the relationship between circ_ 0061140 and miR-6838-5p. Results The expression level of circ_ 0061140 in the non-small cell lung cancer tissues and the cell lines NCI-H1299, NCI-H2170, NCI-H1975 were all higher than that in the adjacent tissues and the BEAS-2B normal lung epithelial cells, while the expression level of miR-6838-5p in the non-small cell lung cancer tissues and the lung cancer cells was lower than that in the adjacent tissues and BEAS-2B cells (all P < 0. 05). the expression level of cyclin D1 protein, the proliferation rate, and the ratio of S phase cells in cells of the si-circ_ 0061140 group and the miR-6838-5p group were lower than those of the NC group, while the expression level of cleaved-caspase-3 protein, the ratio of G0 / G1 phase cells, the apoptosis rate, and the mortality rate were higher than those of the si-NC group and the miR-NC group when compared with the NC group (all P< 0. 05). circ_ 0061140 targeted regulates the expression of miR-6838-5p. Co-transfection of anti- miR-6838-5p and si-circ_ 0061140 could attenuate the effect of si-circ_ 0061140 on the proliferation, cell cycle and apoptosis in non-small cell lung cancer cells. Conclusion The down-regulation of circ _ 0061140 in non-small cell lung cancer cells can suppress the proliferation of cells, block the cells in the G0 / G1 phase, and increase the apoptosis of cells by targeting miR-6838-5p.

Objective To explore the effect of silencing NEK2 on the biological behavior of non-small cell lung cancer (NSCLC) cells and its possible mechanism. Methods A total of 27 pairs of NSCLC and adjacent normal tissues were collected, the expression level of NEK2 in those tissues were detected immunohistochemically, and the clinicopathological data were collected. Bioinformatics methods were performed to analyze the expression level and the prognostic value of NEK2 in lung adenocarcinoma. NCI-H1299 and A549 cells were transfected with siRNA to knock down the expression of NEK2 in vitro, and the knockdown efficiency was assessed by Western blotting and qPCR experiments. CCK-8 was used to measure the proliferation rate of cells, and flow cytometry was used to detect the cell apoptosis and cell cycle. Western blotting was used to detect the expression levels of Wnt signaling pathway related proteins. Results The expression level of NEK2 in lung adenocarcinoma tissues was significantly higher than that in the adjacent tissues, and its expression level in the ⅡB-ⅢB group was significantly higher than that in the IA-ⅡA group. The data obtained from the TCGA database also showed that the expression level of NEK2 in patients with lung adenocarcinoma was significantly higher than that in patients of the corresponding control group, and that its high expression level was significantly associated with a poor prognosis. Transfection of NEK2 siRNA significantly inhibited the proliferation and enhanced the apoptosis of NCI-H1299 and A549 cells, made the cells been arrested in the G0 / G1 phase. In addition, the expression levels of Wnt and β-catenin were significantly lower in the NCI-H1299 and A549 cells transfected with NEK2 siRNA, while the expression level of p-GSK3β was higher. Conclusion Silencing of NEK2 by siRNA can inhibit the proliferation of non-small cell lung cancer cells, the mechanism may relate to the promotion of cell apoptosis and cell cycle arrest through the inhibition of the Wnt / β-catenin pathway.

Objective To observe the protective effect of peroxisome proliferator-activated receptor γ (PPAR-γ) overexpression against renal ischemia-reperfusion (RI/ R) injury in rats, and explore its mechanism. Methods A total of 40 SD rats were randomly divided into 4 groups as follows: the control group, the RI/ R model group, the RI/ R + LV group and the RI/ R + PPAR-γ group, 10 cases in each group. The blood flow of bilateral renal artery was blocked by surgery to construct the RI/ R injury model. Before reperfusionrecovery, rats in the RI/ R + PPAR-γ group were injected with PPAR-γ recombinant lentiviral vector through the tail vein, rats in the RI/ R + LV group were injected with the lentiviral vector containing empty plasmid, while rats in the RI/ R model group wereinjected withnormal saline. After reperfusion, pathological changes in renal tissues were observed by HE staining and Masson staining. The levels of urine protein, serum creatinine (Scr) and blood urea nitrogen (BUN) were measuredby automatic biochemical analyzer. The levels of tumor necrosis factor-α (TNF-α) and interleukin 6 ( IL-6) in serum and renal tissues were determinedby ELISA. The expression level of PPAR-γ mRNA in renal tissues was detected by RT-PCR. The expression levels of PPAR-γ, transforming growth factor β (TGF-β), α-smooth muscle actin ( α-SMA), fibronectin ( FN) and apoptosis-related proteins ( Bax, Bcl-2, caspase-3, Cleaved caspase-3, caspase-9, Cleaved caspase-9) in renal tissues were detectedby Western blotting. Results Compared with the control group, levels of PPAR-γ mRNA and protein were decreased in the RI/ R model group (P< 0. 05), while levels of urine protein, Scr, BUN, TNF-α, IL-6, Bax / Bcl-2, cleaved caspase-3 / caspase-3, cleaved caspase-9 / caspase-9, TGF-β, α-SMA and FN were increased (P< 0. 05). Compared with the RI/ R model group, levels of PPAR-γ mRNA and protein were increased in the RI/ R + PPAR-γ group (P< 0. 05), while levels of urine protein, Scr, BUN, TNF-α, IL-6, Bax / Bcl-2, cleaved caspase-3 / caspase-3, cleaved caspase-9 / caspase-9, TGF-β, α-SMA and FN were decreased (P < 0. 05). Conclusion Overexpression of PPAR-γ can improve renal fibrosis by reducing the release of pro-inflammatory cytokines, thus decreasing RI/ R injury.

Objective To study the role of reactive oxygen species (ROS) -mediated oxidative stress and pyroptosis in the cerebral ischemia-reperfusion (I/ R) injury in rats. Methods Adult male SD rats were divided into 5 groups as follows: the sham group, the I/ R group, the ROS scavenger N-acetylcysteine low dose (NAC-L) group, the NAC medium dose (NAC-M) group and the NAC high dose (NAC-H) group. The cerebral I/ R injury model was established and 50, 100 and 200 mg / kg NAC were injected intraperitoneally before ischemia and reperfusion as an intervention. The neurological function was evaluated 24 h after reperfusion, the percentage of cerebral infarction area, and the levels of ROS, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE) and total antioxidant capacity (T-AOC) were measured. The expression levels of cleaved caspase-1 and N-terminal of gasdermin D (GSDMD-N) were detected. Results In the I/ R group, the percentage of cerebral infarction area, the amount of ROS, MDA, 4-HNE, and the expression levels of cleaved caspase-1 and GSDMD-N were significantly increased, while the amount of T-AOC was significantly decreased (P< 0. 05). In the NAC-L, NAC-M and NAC-H groups, the percentage of cerebral infarction area, the amount of ROS, MDA, 4-HNE, and the expression levels of cleaved caspase-1 and GSDMD-N were significantly decreased, while the amount of T-AOC was significantly increased (P< 0. 05). The changes of the above indexes became more obvious with the increase of the NAC dose. Conclusion ROS mediated oxidative stress and pyroptosis are involved in the cerebral I/ R injury in rats.

Objective To investigate the effect of astragalus polysaccharides on human periodontal ligament stem cells ( PDLSCs) and the related mechanisms by regulating microRNA-375 (miR-375). Methods In this study, human PDLSCs were isolated and cultured in vitro. Cells were treated with 0, 40, 100, 400 μg / mL astragalus polysaccharide for 48 h. Cells in the astragalus polysaccharides + anti-miR-NC group and astragalus polysaccharides + anti-miR-375 group were transfected with anti-miR-NC and anti-miR-375 respectively, and treated with 400 μg / mL astragalus polysaccharides for 48 h. Alkaline phosphatase (ALP) activity were measured and the proliferation of PDLSCs was assayed by using methylthiazolyldiphenyl-tetrazolium bromide (MTT). The expression levels of Runt-related transcription factor 2 (Runx-2), osteopontin (OPN) and osteocalcin (OCN) were detected by Western blotting. The expression level of miR-375 was detected by real-time quantitative polymerase chain reaction (qRT-PCR). Results Astragalus polysaccharide can promote the expression of miR-375 [ (1. 54 ±0. 16, 1. 92 ±0. 20, 2. 54 ±0. 22) of the astragalus polysaccharide groups vs. (0. 92 ±0. 07) of the control group] . Astragalus polysaccharide treatment promoted the proliferation of PDLSCs, the A values were (0. 46 ±0. 05, 0. 58 ±0. 07, 0. 72 ± 0. 06) of the astragalus polysaccharide groups vs. (0. 35 ±0. 04) of the control group for 48 h treatment, and (0. 53 ±0. 05, 0. 69 ±0. 07, 0. 84 ±0. 09) of the astragalus polysaccharide groups vs. (0. 40 ±0. 03) of the control group for 72 h. The values for ALP activity were (0. 73 ±0. 08, 0. 84 ±0. 07, 1. 03±0. 09) of the astragalus polysaccharide groupsvs. (0. 32 ±0. 03) of the control group. Treatment with various concentrations of astragalus polysaccharide also up-regulated the expression of Runx-2 [ (1. 32 ±0. 11, 1. 51 ±0. 14, 1. 83 ±0. 17) vs. (0. 92 ±0. 07)], OCN [ (1. 47±0. 13, 1. 65 ±0. 16, 1. 89±0. 19) vs. (0. 99±0. 06)], OPN [ (1. 53 ±0. 15, 1. 72 ± 0. 16, 1. 99 ±0. 20) vs. (1. 00±0. 04)] . The expression level of miR-375, cell proliferation, ALP activity, and the expression levels of Runx-2, OCN, OPN of astragalus polysaccharide + anti-miR-375 group were significantly lower than that of the astragalus polysaccharide + anti-miR-NC group. Conclusion Astragalus polysaccharide can promote the proliferation and osteogenic differentiation of human periodontal ligament stem cells, and its mechanism may be related to miR-375.

Objective To explore the clinical and prognostic value of serum exosomal LncRNA HOTTIP in patients with breast cancer (BC). Methods Exosomes were extracted from serum samples of 98 BC patients, 50 benign breast disease (BBD) patients and 50 healthy subjects by kit, and the expression level of HOTTIP in the serum exosomes was detected by RT-qPCR. Furthermore, the relationship among the expression level of HOTTIP, the clinicopathological features and the overall survival was analyzed. Results The expression level of HOTTIP in serum exosomes of the BC patients was significantly higher than that of the BBD patients (t = 8. 790, P< 0. 001) and that of the normal healthy people (t = 11. 540, P< 0. 001), and the level of HOTTIP in serum exosomes of the BC patients significantly decreased after surgery ( t = 14. 570, P < 0. 001 ) . Clinicopathological analysis showed that high serum exosomal HOTTIP level was significantly correlated with HER2 expression level, lymph node metastasis and TNM stage ( all P < 0. 05). Further survival analysis showed that the 5-year survival rate of BC patients in the high serum exosomal HOTTIP expression group was significantly lower than that in the low HOTTIP expression group (χ 2 = 5. 548, P = 0. 019). Moreover, multivariate analysis demonstrated that high expression level of serum exosomal HOTTIP was an independent risk factor for the poor prognosis of BC (HR = 2. 454, 95 % CI: 1. 142-7. 005, P = 0. 031 ). Conclusion The expression of serum exosomal lncRNA HOTTIP is up-regulated in BC, and its high expression indicates the malignant progression of cancer and poor prognosis of BC patients, which implies that serum exosomal lncRNA HOTTIP could be a non-invasive biomarker for the the assessment of prognosis in BC patients. 

Protein glycosylation is a wide range of post-translational modifications, with the involvement of the synthesis of different polysaccharide cores and the attachment of which to particular amino acids within a protein consensus sequences. Most glycoproteins acquire glycosyl groups from the secretory system includes endoplasmic reticulum and Golgi apparatus, they are then secreted to the plasma membrane-associated cell wall or extracellular spaces. Glycosylation can regulate the function of glycoproteins by affecting their folding, sorting, localization, abundance and activity in cells. In recent years, many studies have reported that glucose metabolism have an effect on the protein glycosylation. This paper reviews the relationship between hexosamine biosynthesis pathway and the protein glycosylation. 

Although kidney transplantation is the best choice for the treatment of end-stage renal disease, immune rejection after transplantation is still a major clinical problem and acute rejection is the most common immune rejection after transplantation. Transplantation medicine is facing a demand for new specific biomarkers in the preventive screening, early diagnosis, and the improving of prognosis and treatment. At present, proteomics has been widely used in the research of transplantation medicine, and a great progress has been made on the screening of biomarkers related to acute rejection after renal transplantation in serum and urine. This article reviews the research progress of screening of biomarkers related to acute rejection after renal transplantation by using proteomics based on mass spectrometry. 

In recent years, more and more people suffer from myopia. Myopia has become a major concern in China with the characteristic of serious complications accompanied and a trend of younger age. Several studies have shown that abnormal changes occur in the wall of eyeball as myopia progresses. In this paper, the abnormal changes in the wall of eyeball with myopia and their molecular mechanisms is reviewed to provide a basis for the further research on myopia and the prevention and control of it.