High Endplate Hounsfield Units Value Indicate Intervertebral Disc Degeneration Following Transforaminal Lumbar Interbody Fusion Surgery

Objective

Lumbar disc degeneration (LDD) is a common cause of low back pain and disability, and its prevalence increases with age. The aim of this study is to investigate whether endplate Hounsfield unit (HU) values have an effect on lumbar disc degeneration (LDD) after transforaminal lumbar interbody fusion (TLIF) surgery in patients with degenerative lumbar stenosis.

Methods

This study was a retrospective analysis of patients who underwent TLIF surgery in January 2016 to October 2019. One hundred and fifty-seven patients who underwent TLIF surgery for degenerative lumbar stenosis were enrolled in this study. Demographic data was recorded. VAS and ODI values were compared to assess the surgical outcomes in patients with or without process of LDD after TLIF surgery. Correlation analysis was performed to investigate associations between LDD and endplate HU value. Binary logistic regression analysis was carried out to study relationships between the DDD and the multiple risk factors.

Results

There was a statistically significant correlation between LDD, body mass index (BMI), age, paraspinal muscle atrophy, and total endplate scores (TEPS). Also, a strong and independent association between endplate HU value and LDD was found at every lumbar disc level (p < 0.01). After conditioning on matching factors, multivariate logistic regression analysis showed that higher endplate HU (odds ratio [OR]: 1.003, p = 0.003), higher TEPS (OR: 1.264, p = 0.002), higher BMI (odds ratio [OR]: 1.202, p = 0.002), a smaller cross-sectional area (CSA) of the paraspinal muscle preoperatively (OR: 0.096, p < 0.001) were significant predictors of LDD development after TLIF surgery.

Conclusions

There is a significant association between LDD and endplate HU value after TLIF surgery in patients with degenerative lumbar stenosis. Beyond that, results from this study provide a mechanism by which high endplate HU value predisposes to LDD after TLIF surgery.     

乙醇对蟾蜍神经-肌接头传递的影响

目的　研究乙醇对神经肌肉接头 (NMJ)兴奋传递的影响及可能机制。方法　用微电极细胞内记录的方法 ,在 2 0只成年蟾蜍的坐骨神经 -缝匠肌标本上研究乙醇对终板电位 (EPP)和微小终板电位 (MEPP)的影响。结果　乙醇可引起 EPP振幅改变 ,影响 NMJ的兴奋传递 ,而且其影响具有明显的量效依赖关系 ,适当浓度的乙醇能明显地增加 EPP振幅 ,促进 NMJ的兴奋传递。乙醇还可使 MEPP的频率增加 ,但对 MEPP的振幅无影响。结论　初步确定乙醇促进 NMJ兴奋传递的部位是在突触前 ,其机制是使突触前释放的递质的量子数增加     

SIRT1 targeted by miR-211-5p regulated proliferation and apoptosis of Dex-treated growth plate chondrocytes via mediating SOX2

Dexamethasone (Dex) is reported to cause bone growth retardation in children, which is associated with the increased apoptosis and decreased proliferation of growth plate chondrocytes. Sirtuin 1 (SIRT1) plays an important role in chondrocyte function and homeostasis. Thus, we further explored the regulatory mechanism of SIRT1 in Dex-induced growth plate chondrocyte dysfunction. SIRT1 expression was detected in Dex-treated growth plate chondrocytes using RT-qPCR and western blot assay. The modulation of SIRT1 on SOX2 expression was evaluated. Besides, we identified that SIRT1 was targeted by miR-211-5p using TargetScan and RNA pull-down assay. A loss-of-function assay was performed to evaluate the effects of miR-211-5p on Dex-induced growth plate chondrocyte dysfunction in vitro and in vivo. We found that SIRT1 was downregulated in Dex-treated growth plate chondrocytes. The expression of SOX2 was upregulated by overexpression SIRT1. Meanwhile, downregulation of SOX2 weakened the positive function of SIRT1 overexpression on Dex-induced growth plate chondrocytes dysfunction. Subsequently, we confirmed that SIRT1 was targeted by miR-211-5p. MiR-211-5p inhibitor increased the expression levels of SIRT1 and SOX2, and restored the Dex-treated growth plate chondrocyte function. Animal assays further demonstrated that the effects of miR-211-5p on the growth plate chondrogenesis. In conclusion, our data suggest that SIRT1 exerts a protective effect on growth plate chondrocyte under Dex stimulation. MiR-211-5p/SIRT1/SOX2 axis regulates the process of Dex-inhibited growth plate chondrogenesis.     

Baicalin mitigated IL-1β-Induced osteoarthritis chondrocytes damage through activating mitophagy

Mitophagy is related to chondrocyte homeostasis and plays a key role in the progress of osteoarthritis (OA). Baicalin has a protective effect on OA chondrocytes, the aim of this study was to explore whether the effect of Baicalin on IL-1β-induced chondrocyte injury is related to the regulation of mitophagy. The expression of collagen II in chondrocytes was detected to identify chondrocytes. The effects of different concentrations of Baicalin (10, 20 and 40 μM), autophagy inhibitor (3-Methyladenine), autophagy activator (rapamycin) and Baicalin combined with PI3K agonist (740Y-P) on the viability (cell counting kit 8), apoptosis (flow cytometry), autophagy activation (Monodansylcadaverine staining) and mitochondrial membrane potential (JC-1 kit) of IL-1β-induced chondrocytes were evaluated. The co-localization of autophagosome and mitochondria was determined by immunofluorescence. Apoptosis-, autophagy-, PI3K/AKT/mTOR pathway- and mitophagy-related proteins were detected by western blot. Our result revealed that Baicalin and rapamycin facilitated cell viability, autophagy and mitophagy, elevated mitochondrial membrane potential and suppressed apoptosis of IL-1β-induced rat chondrocytes. In addition, Baicalin and rapamycin upregulated the levels of Bcl-2, Beclin 1, LC3-II/LC3-I, p-Drp1, PINK1 and Parkin as well as downregulated the levels of Bax, cleaved caspase-3, P62, p-PI3K/PI3K, p-mTOR/mTOR and Drp1 in IL-1β-induced rat chondrocytes. However, 3-Methyladenine did the opposite effects of Baicalin and 740Y-P reversed the effects of Baicalin on IL-1β-induced rat chondrocytes. In conclusion, Baicalin activated mitophagy in IL-1β-induced chondrocytes by inhibiting PI3K/AKT/mTOR pathway and activating PINK1/Parkin and PINK1/Drp-1 pathway, thereby reducing the chondrocyte injury.     

软骨细胞线粒体生物发生在骨关节炎发病机制中的作用北大核心CSCD

目的总结软骨细胞线粒体生物发生在骨关节炎(osteoarthritis,OA)发病机制中的作用并分析其应用前景。方法查阅近年国内外相关文献,对线粒体生物发生在OA病程中的变化、在OA软骨细胞中主要信号分子的作用,以及在OA治疗中的应用前景进行总结。结果近年研究发现线粒体是软骨细胞的重要能量代谢中心,其功能障碍被认为是OA发生、发展的重要机制。线粒体生物发生是维持线粒体正常数量和功能的关键生物过程之一,过氧化物酶体增殖物激活受体γ辅激活因子1α(peroxisome proliferator-activated receptor-gamma coactivator 1 alpha,PGC-1α)是该过程的关键调控因子。现已报道了以PGC-1α为中心,腺苷酸活化蛋白激酶、沉默信息调节因子1/3及环磷酸腺苷反应元件结合蛋白等为主要上游调控分子,核呼吸因子1、雌激素受体α、核呼吸因子2等为主要下游调控分子的线粒体生物发生调控网络。然而,软骨细胞线粒体生物发生在OA发病机制中的作用还需进一步深入探索。已有研究表明如葛根素、人网膜素-1等药物和活性物质可通过激活OA软骨细胞中受损的线粒体生物发生过程延缓OA发生、发展,为OA治疗提供了新思路。结论软骨细胞线粒体生物发生在OA发病机制中起重要作用,进一步探索相关机制具有重要临床意义。