Objective To explore the effects and mechanism of cigarette smoke extract (CSE) on the proliferation of air?way smooth muscle cells (ASMCs) and the expression of CCAAT/enhancer-binding protein (CEBPα) and calreticulin. Meth?ods (1) The ASMCs were stimulated with different concentrations of CSE for twenty-four hours. According to the concentra?tions of CSE,the cells were divided into control group, 2.5%CSE group, 5%CSE group and 10%CSE group. The prolifera?tion of ASMCs was measured by MTT colrimetric method. The CEBPαmRNA was analyzed by RT-PCR. Western bloting as?say was performed to detect the levels of CRT and CEBPαprotein. (2) In 10%CSE group, transfection of the siRNA respec?tively for negative control or calreticulin was performed in accordance with instructions. The cell proliferation and the expres?sion of calreticulin and CEBPαwere compared in negative control siRNA group and calreticulin siRNA group. Results (1) With the increasing of the concentrations of CSE, the protein expression of CEBPαdecreased gradually (P<0.05), while the proliferation of ASMCs and the protein expression of calreticulin increased (P<0.05), but the expression of CEBPαmRNA in ASMCs showed no significant difference in groups with different concentrations of CSE (P>0.05). (2) Under the 10%CSE, the expression of CEBPαwas significantly higher in CRT siRNA group than that in negative control group (P<0.05),but the cell proliferation and CRT were significantly lower in the calreticulin siRNA group than those in negative control siRNA group (P<0.05). Conclusion The CSE exposure contributes to the expression of calreticulin protein,and then inhibits the translation of CEBPαmRNA,thus promotes the proliferation of ASMCs.

BACKGROUND:Transformation growth factor-β(TGF-β) and brain-derived neurotrophic factor (BDNF) are the main regulatory factors in the process of spinal cord injury. There are many researches for TGF-βand BDNF pathogenesis in the spinal cord injury, but the regulation of Ginsenoside Rg1 intervention on TGF-βand BDNF in the spinal cord injury is rarely reported.
OBJECTIVE:To observe the effect of Ginsenoside Rg1 intervention on TGF-βand BDNF expression at themolecular protein levels, and to study the protection effect of Ginsenoside Rg1 on the spinal cord and nerve function after spinal cord injury.
METHODS:Experimental rats were randomly divided into blank control group, model group and Ginsenoside Rg1 group. In the model and Ginsenoside Rg1 groups, spinal cord injury model was established with the impact method in rats. In the Ginsenoside Rg1 group, rats were intraperitoneal y injected with 10 mg/kg Ginsenoside Rg1 24 hours after modeling, once per day, for 14 days. Rats in the blank control and model groups were injected with equal saline.
RESULTS AND CONCLUSION:Compared with the control group, serum malondialdehyde levels increased, the content of superoxide dismutase decreased, TGF-βexpression levels in spinal cord tissue increased, and BDNF expression levels decreased in the model and Ginsenoside Rg1 groups. Compared with the model group, serum malondialdehyde levels decreased, the content of superoxide dismutase increased, TGF-βexpression levels in spinal cord tissue decreased, and BDNF expression levels increased in the Ginsenoside Rg1 group. Ginsenoside Rg1 can protect the injury spinal cord in rats after spinal cord injury.

BACKGROUND:Chinese herb extracts can restore and protect the nervous system of rats through intervention of neural stem cels. OBJECTIVE:To explore the role of ginsenosides Rg1 in the proliferation and protection of neural stem cels. METHOD:Sprague-Dawley rats at pregnant 19 days were dissected to take out fetal rats, and then the hippocampal tissues from fetal rats were isolated to extract neural stem cels. Neural stem cels were co-cultured with DMEM/F12 medium containing 50 g/L ginsenosides Rg1 as intervention group, with DMEM/F12 medium as blank control group, and with DMEM/F12 containing 0.64% phenol as positive control group, respectively. MTT assay was used to detect the proliferation of neural stem cels in each group, and western blot method to detect the protein expression of brain-derived neurotrophic factor and transforming growth factor-β in neural stem cels. RESULTS AND CONCLUSION:Rat neural stem cels were round single cels with clear border at early period after isolation but at 2 days after inoculation, the cels were adherent and aggregated into smal cel spheres. Compared with the blank control group, the proliferative rate of neural stem cels was significantly increased in the ginsenosides Rg1 group (P < 0.05), but decreased in the positive control group (P < 0.05). Compared with the blank control group, in the ginsenosides Rg1 group, the expression of brain-derived neurotrophic factor was elevated, and the expression of transforming growth factor-β was reduced, indicating ginsenosides Rg1 has a certain effect to promote the proliferation of neural stem cels as wel as to protect the neural stem cels.

Objective To evaluate the mechanical stability of alternative reconstruction methods after total en bloc spon?dylectomy in the lower lumbar spine. Methods Eight adult fresh cadaveric lumbosacral spines (L1-S1) were adopted. Total en bloc spondylecotmy of the L4 vertebra was performed after intact testing. Four designed reconstruction samples were tested for the range of motion (ROM) of the spine:1) expandable artificial vertebral body and short posterior instrumentation at L3-L5 (SP), 2) ex?pandable artificial vertebral body and short posterior instrumentation with additional anterolateral fixation at L 3-L5 (ASP), 3) ex?pandable artificial vertebral body and multilevel posterior instrumentation at L2-S1 (MP), 4) expandable artificial vertebral body and multilevel posterior instrumentation with additional anterolateral fixation at L2-S1 (AMP). Nondestructive biomechanical test?ing was performed on each construct under loading control. The ROM for each construct was obtained by applying pure moments in flexion, extension, lateral bending, and axial rotation. Results In flexion, extension and lateral bending, the ROM of all the re?constructed constructs significantly decreased compared to the intact. The ROM of specimens with anterolateral fixation was less when compared to the ones without additional fixation. In lateral bending, MP (L:1.87° ± 0.32° , R:1.97° ± 0.33° ), ASP (L:1.89° ± 0.37°, R:2.08°±0.36°) and AMP (L:1.32°±0.29°, R:1.61°±0.33°) provided significantly less ROM than the SP (L:3.14°±0.35°, R:3.44°±0.34°). In axial rotation, the ROM of ASP (L:4.21°±0.58°, R:4.02°±0.59°) and AMP (L:3.56°±0.55°, R:3.52°±0.48°) was significant decreased when compared to the intact state (L: 7.47° ± 1.00° , R:7.57° ± 0.84° ). MP (L:6.33° ± 0.71° , R:5.88° ± 0.62°), ASP and AMP showed significantly less ROM than the short posterior fixation (L:9.28°±1.01°, R:9.48°±0.98°). AMP sig?nificantly decreased the ROM compared to MP. Conclusion After total en bloc spondylectomy of lower lumbar, long segmental fixation provided more stability to the construct than the short one. Compared to posterior fixation, circumferential fixations showed a higher stability. In contrast, multilevel segmental instrumentation with circumferential fixation did not provided more stability than the short constructs.

Low back pain (LBP) is closely related to intervertebral disc degeneration (IDD) , spinal canal stenosis, intervertebral disc herniation, osteoarthritis of intervertebral facet joints, ligament and muscle lesions, among which IDD is the key factor causing low back pain. Emerging evidence suggests that a large number of pro-inflammatory cytokines are produced during IDD, and the inflammatory responses induced by these cytokines aggravate the occurrence and development of degeneration. At the molecular level, the mechanism of regulating intervertebral disc metabolism based on signal pathway has become a research hotspot, but the specific pathway mechanism is still unclear. In this paper, according to the crosstalk of NF-κB, TGF-β, MAPK, Wnt/β-catenin, PI3K/AKT/mTOR and other signal pathways, the positive and negative feedback effects of signal pathways on the inflammatory response during disc degeneration will be discussed. To elucidate the pro-inflammatory effects of NF-κB, anti-inflammatory effects of TGF-β and MAPK as well as the potential mechanisms of other pathways, we analyze the internal relationship between the mechanism of IDD and the signal pathway transduction, in order to provide new ideas for the treatment of IDD.