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[Subcostal abscess following laparoscopic cholecystectomy].
Results The expression of UNC5B-AS1 in lung cancer tissues and cells was significantly higher than that in adjacent tissues and bronchial epithelial cells (P＜0.05). The expression of UNC5B-AS1 in lung cancer A549 cells was the highest (P＜0.05). Down-regulation of UNC5B-AS1 expression inhibited adhesion, invasion and migration of A549 cells (P＜0.05). qRT-PCR and dual luciferase reporter assay experiments showed that UNC5B-AS1 targeted the regulation of miR-218-5p expression. Down-regulation of UNC5B-AS1 inhibited E-cadherin protein expression and promoted Vimentin and Twist protein expression. Conclusion lncRNA UNC5B-AS1 promotes adhesion, invasion and migration of lung cancer cells through targeted regulation of miR-218-5p expression, and its mechanism may be related to the promotion of EMT.Objective To investigate the toxic effects of vitamin C (VC) combined with temozolomide (TMZ) on gliomas and its mechanism. Methods Human glioma cells BMG-1 and SHG44 cells were cultured in vitro, specifically divided into control group (without VC and TMZ), TMZ group (0.2 mmol/L), VC (0.5 mmol/L)+TMZ(0.2 mmol/L) group and TMZ(0.2 mmol/L TMZ)+U0126(10 μmol/L)group, each experiment was repeated three times. Cell survival rate was detected by MTT assay; Cell apoptosis was detected by flow cytometry and Annexin V-FITC/PI staining; Reactive oxygen species (ROS) levels were detected by ROS detection kit, and Western blot was used to detect the expression levels of proteins related to apoptosis, autophagy and ERK pathway. Results Compared with the control group, the survival rate of glioma cells in the TMZ group was decreased significantly(P＜0.05). Compared with the TMZ group, the survival rate of glioma cells in the VC+TMZ group was decreased significantly(P＜0.01), the cell apoptosis rate was increased, and the expressions of Bax, Cleaved caspase-3 and Cleaved PARP protein were increased, while the expression of Bcl-2 was decreased. Picropodophyllin in vivo The ROS level and autophagy rate were decreased, while the expression of LC3-II/LC3-1 was decreased, and the expression of p62 was increased in the VC+TMZ group (all P＜0.05). At the same time, VC combined with TMZ decreased the expression level of p-ERK1/2-related protein in BMG-1 and SHG44 cells, and increased the apoptosis rate (P＜0.05). Conclusion VC combined with temozolomide can enhance the toxicity of glioma cells. This effect is to promote apoptosis and inhibit temozolomide-mediated autophagy through the regulation of the ERK signaling pathway.Objective To explore the role and mechanism of polysaccharide-1 (syndecan-1) in the transformation of lung epithelial stroma (EMT) in rats with chronic obstructive pulmonary disease (COPD). Methods Thirty male SD rats of clean grade were randomly divided into sham operation group (normal saline injection after tracheal exposure, n=10), COPD group (fumigation after injection of 1 mg/ml lipopolysaccharide, transfection of 100 μl empty virus, n=10) and syndecan-1 overexpression group (fumigation after injection of 1 mg/ml lipopolysaccharide, and transfection of 100 μl carrying rat syndecan-1 gene Ad-CMV-GFP-SDC1, n=10), once a day for two weeks. After the treatment, the lung function was detected and lung tissues were collected. HE staining was used to observe lung injury. The expression levels of syndecan-1, vimentin and E-cadherin in lung tissue of rats in each group were detected by immunohistochemistry. Western blot was used to detect the expressions of TGF-β1, Smad2/3 and p-Smad2/3. The mRNA levels of vimenrotein were significantly decreased (P＜0.05). Conclusion In COPD rats, TGF-β/Smad signal pathway activation induced the production of EMT; overexpression of syndecan-1 could inhibit the EMT mediated by TGF-β/Smad signal pathway, and improve the lung tissue injury of COPD rats.Objective To investigate the effects of Bushen Zhuanggu granule on the expressions of serum growth hormone (GH) and insulin-like growth factor-1(IGF-1) and their receptors in bone tissues of ovariectomized rats. Methods Forty-eight SD female rats (weight 273±21.3 g) were divided into 4 four groups the dosage of Bushen Zhuanggu granule group (BSZG) was 2.5 g/(kg·d),the do -sage of estradiol group(E2) was 0.071mg/(kg·d),sham group (SHAM) and ovariectomized model group (OVX group) were given the same amount of saline by oral administration.Each group included 12 rats,the treatments were conducted once a day. After 3 and 6 months of treatment,bone mineral density (B -MD) was measured by bone density instrument;the serum levels of GH and IGF-1 were detected by EL-ISA;the expressions of GHR and IGF-1R of bone tissue were detected by qPCR;the optical density(OD)value and positive cell count of pituitary GH immunohistochemical tablets were analyzed by Image J software,respectively. Results ①After 3 months interventioGF-1 in serum and its receptors in bone tissues of ovariectomized osteoporosis rats to prevent further loss of bone mass and increase bone mineral density.Objective To study the expression and correlation of mir-203a and its target gene ATM in breast cancer tissues, so as to provide theoretical basis for the pathogenesis of breast cancer, especially lymph node metastasis. Methods Thirty paired breast cancer and paracancer normal tissues were collected, and RT-qPCR was used to detect the relative expression levels of mir-203a and ATM in the samples of the two groups. Correlation analysis was conducted for mir-203a and ATM, and correlation analysis was conducted for the pathological characteristics, so as to compare whether there were statistical differences between mir-203a and ATM in lymph node metastasis and non-metastasis. Results Compared with normal paracancer tissues, the expression level of mir-203a in breast cancer tissues was significantly increased (P＜0.01), and the expression level of ATM was significantly decreased (P＜0.01), showing a significant negative correlation between the two tissues (r=-0.847,P＜0.01).The expression level of mir-203a and ATM was significantly correlated with lymph node metastasis and different clinical stages (P＜0.05). The expression level of mir-203a in the group with lymph node metastasis were significantly lower than that in the group without lymph node metastasis (P＜0.05), and the expression of ATM in the group with lymph node metastasis was significantly higher than that in the group without lymph node metastasis (P＜0.01). Conclusion The overexpression of mir-203a in the early stage of breast cancer may inhibit the expression of its target gene ATM, which may be a protective mechanism to regulate the proliferation,metastasis and invasiveness of tumor cells. In the middle and late stage, mir-203a is down-regulated and the ATM gene is up-regulated, which may be involved in lymph node metastasis.
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