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08 December 2020, Volume 24 Issue 在线 Previous Issue    Next Issue

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Triptolide improves spinal cord injury recovery via upregulation of autophagy and inhibition of apoptosis in Thy-yfp transgenic mice Zhu Ning, Yang Xinming, Ruan Jianwei 2020, 24 (在线):  1.  Abstract ( 371 )   PDF (898KB) ( 128 )   Save BACKGROUND: Studies have shown that treatment with triptolide reduces ischemic lesion area, water content, and nerve cell death in a rat model of stroke. In addition, triptolide can promote the repair of spinal cord injury by inhibiting astrocyte hyperplasia, microglia activation and inflammatory response. OBJECTIVE: To investigate the effect of triptolide on the autophagy and apoptosis in the spinal cord of Thy-YFP transgenic mice after spinal cord injury. METHODS: Sixty Thy-YFP transgenic mice were randomly divided into four groups: sham, dimethyl sulfoxide (DMSO), triptolide and methylprednisolone groups. Following the establishment of the spinal cord injury models, mice in the triptolide, DMSO and sham group were immediately intraperitoneally injected with triptolide (0.2 mg/kg·d) or 5% DMSO-normal saline solution (0.2 mg/kg·d) for 7 days, whereas mice in the methylprednisolone group were intraperitoneally injected with methylprednisolone (30 mg/kg) at 30 minutes, 6 hours and 24 hours after surgery. BMS score was used to detect the recovery of motor function; hematoxylin-eosin staining and Nissl staining were used to explore tissue recovery after spinal cord injury; western blot and immunofluorescence staining were employed to assess the levels of autophagy-associated proteins, Beclin-1, LC3B, p62, and apoptosis-associated proteins, Bcl-2, Bax and caspase-3. An ethic approval for animal experiments was obtained from Hebei North University with an approval No. W20200002. RESULTS AND CONCLUSION: Treatments with triptolide or methylprednisolone after spinal cord injury significantly improved motor function and reduced neuronal cell death. In addition, autophagy-associated protein LC3B was upregulated and p62 downregulated following triptolide treatment, apoptosis-associated proteins caspase-3 and Bax were reduced, while anti- apoptosis protein Bcl-2 was increased after triptolide treatment. To conclude, triptolide improves the motor function after spinal cord injury, which is related to upregulation of autophagy and inhibition of apoptosis. Triptolide may be a potential neuroprotective agent for spinal cord injury. Related Articles | Metrics

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Effects of ultrashort wave on inflammatory response in rats with acute lung injury Liao Yuan, Qu Mengjian, Liu Jing, Zhong Peirui Zeng Yahua, Wang Ting, Xiao Hao, Li Lan, Liu Danni, Yang Lu, Zhou Jun 2020, 24 (在线):  2.  Abstract ( 248 )   PDF (715KB) ( 134 )   Save BACKGROUND:  Ultrashort wave can inhibit the inflammatory response and is often used in symptomatic treatment of pulmonary infection. Uncontrolled inflammatory response is an important pathogenesis of acute lung injury. Inhibiting inflammation is an important strategy for controlling acute lung injury. OBJECTIVE: To observe the effects of ultrashort wave on inflammatory response and the expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in rats with acute lung injury. METHODS: Twenty-four 3-month-old male Sprague-Dawley rats were randomly divided into control group, acute lung injury group (model group) and ultrashort wave group (n=8 per group). Rats in the acute lung injury group and the ultrashort wave group were given intratracheal lipopolysaccharide to replicate the acute lung injury model. Rats in the control group were given intratracheal infusion of the same amount of normal saline. In the ultrashort wave group, rats were given ultrashort wave intervention immediately, 4 and 8 hours after lipopolysaccharide infusion, once for 15 minutes. Experimental animals were sacrificed 24 hours after intratracheal infusion of lipopolysaccharide or normal saline. The lung tissues of rats were compared by hematoxylin-eosin staining, lung histopathological semi-quantitative score and lung wet/dry weight ratio (W/D). Serum levels of inflammatory factors TNF-α and IL-1β were detected by ELISA, and mRNA and protein expressions of TNF-α and IL-1β were detected by RT-PCR and western blot, respectively. RESULTS AND CONCLUSION: Lung W/D ratio in the acute lung injury group was significantly higher than that in the control group (P < 0.01), whereas the ratio in the ultrashort wave group was lower than that in the acute lung injury group, but there was no significant difference between the two groups. Pathological manifestations: In the model group, the lung tissue structure was obviously damaged, with different sizes of alveolar septa, the alveolar wall was incomplete, thickened and fractured, a large number of neutrophils were seen in the lung interstitium, and some red blood cells were exudated. In the ultrashort wave group, compared with the model group, the alveolar structure was relatively complete and clear, and the infiltration of inflammatory cells and red blood cell exudation from the lung interstitium were reduced. Semi-quantitative histopathological score of the lung was significantly higher in the model group than the control group (P < 0.01), but significantly reduced in the ultrashort wave group compared with the model group (P < 0.01). Serum TNF-α and IL-1β levels in the model group were significantly higher than those in the control group (both P < 0.01). After ultrashort wave exposure, the levels of serum TNF-α and IL-1β significantly decreased compared to the model group (both P < 0.05).  After ultrashort wave exposure, the mRNA and protein expressions of TNF-α and IL-1β significantly decreased compared to the model group (P < 0.01 or P < 0.05). To conclude, ultrashort wave may inhibit the inflammatory response of the lung tissue in rats with acute lung injury by down-regulating the expression of inflammatory cytokines TNF-α and IL-1β.  Related Articles | Metrics

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Efficacy of mesenchymal stem cells in the spinal cord injury of large animal models: a meta-analysis Kong Desheng, He Jingjing, Feng Baofeng, Guo Ruiyun, Asiamah Ernest Amponsah, Lü Fei, Zhang Shuhan, Zhang Xiaolin, Ma Jun, Cui Huixian 2020, 24 (在线):  3.  Abstract ( 255 )   PDF (1503KB) ( 90 )   Save OBJECTIVE: Mesenchymal stem cells transplantation is a promising treatment for spinal cord injury. Most of studies focused on small animal models. In large animal experiments, there are still controversies in selection of stem cells and therapeutic effect. This article analyzed the effects of mesenchymal stem cells on related indicators of spinal cord injury in large animal models and evaluated their effects on spinal cord injury repair.  METHODS: PubMed, Cochrane, OVID, Web of Science and CNKI databases were retrieved before December 2019. A series of studies on the treatment of spinal cord injury in large animal models by mesenchymal stem cells were collected. According to the inclusion criteria, two researchers independently completed literature screening, data extraction and methodological quality evaluation, and meta-analysis was conducted with Stata16.0.  RESULTS: A total of 10 articles were included. The results of meta-analysis showed that: (1) Mesenchymal stem cells could significantly improve motor function after spinal cord injury [I2=97.73%, MD=3.94, 95%CI (2.15, 5.72), P < 0.01]. Based on cell source, observation time, intervention phase, transplantation mode and graft type subgroup analysis showed that motor scores of bone marrow mesenchymal stem cells group, non-bone marrow mesenchymal stem cells group, short-term observation (< 2 months) group, long-term observation (≥ 2 months) group, acute stage group, non-acute stage group, cells group and allograft group were significantly higher than those of control group (P < 0.01). There was no significant difference in motor score between scaffold group and control group (P > 0.05). (2) The injury size in mesenchymal stem cells treatment group was significantly smaller than that in the control group [I2=98.05%, MD=-1.00, 95%CI (-1.95, -0.04), P=0.04]. (3) There was no significant difference in the relative expression of glial fibrillary acidic protein between the mesenchymal stem cells treatment group and the control group [I2=99.48%, MD=80.61, 95%CI (-27.48, 188.70), P=0.14].  CONCLUSION: Mesenchymal stem cells transplantation has a significant improvement on the motor function and injury repair of spinal cord injury, and the security is high. Due to the limitation of the quality of the included literatures, the above conclusions need to be validated by high-quality and large-sample randomized controlled trials. Related Articles | Metrics

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Corylin inhibits osteoclastogenesis and attenuates postmenopausal osteoporosis in mice Li Xiaoqun, Xu Kaihang, Ji Fang 2020, 24 (在线):  4.  Abstract ( 242 )   PDF (728KB) ( 88 )   Save BACKGROUND: The balance of bone homeostasis is mediated by the osteoclast-related bone resorption and osteoblast-related bone formation. Over-activation of osteoclasts results in a series of bone metabolic diseases including rheumatoid arthritis and osteoporosis. The activation of nuclear factor-κB  pathway induced by receptor activator of NF-κB ligand (RANKL) plays an important role in osteoclastogenesis. OBJECTIVE: To explore the effect of corylin on RANKL-mediated osteoclastogenesis.  METHODS: RAW264.7 cells were incubated with 0, 1, 2, 4, 8, 16, 32, 64, 128 μmol/L corylin. The cytotoxicity of corylin was detected by cell counting kit-8 assay. RANKL induced the differentiation of RAW264.7 cells into osteoclasts, during which 2, 5, 10 μmol/L corylin was given. The number of osteoclasts was analyzed by TRAP staining after 5 days of intervention and the morphology and function of osteoclasts were analyzed by F-actin staining. Bone resorption assay was conducted after 2 days of intervention. The activation of NF-κB pathway was detected by western blot at 0, 15, 30, and 60 minutes of intervention. Then in vivo experiments were carried out, and the ovariectomized mice were intraperitoneally given 10 mg/kg twice a week. After 6 weeks of intervention, mouse femurs were taken for morphological analysis. RESULTS AND CONCLUSION: There was no cytotoxicity of corylin below the concentration of 16 μmol/L. Corylin inhibited osteoclastogenesis in a dose-dependent manner. Corylin inhibited the formation of F-actin and resorption activity of osteoclasts. Corylin inhibited RANKL-mediated nuclear factor-κB pathway. Corylin treatment reduced the bone loss in postmenopausal osteoporosis mice. Overall, corylin inhibits osteoclastogenesis via blocking nuclear factor-κB pathway and attenuates postmenopausal osteoporosis.  Figures and Tables | References | Related Articles | Metrics