Assessment of the correlation between clinical and radiological outcomes in patients suffering from mild to moderate cervical spine dysfunction symptoms: a prospective study.

BACKGROUND: Neck pain and cervical disc degeneration (CDD) are common findings. Valid data on correlation between clinical scores and radiological grade of CDD in patients with mild to moderate clinical disability are not available. The study has been designed to investigate the correlation between clinical and radiological outcomes in these patients. METHODS: A cohort of 150 patients who suffered from mild to moderate cervical spine dysfunction symptoms from September 2020 to May 2021 was enrolled. We evaluated functional status using Japanese Orthopaedic Association scores (JOA), the visual analog scale, and the Neck Disability Index. We assessed the CDD with magnetic resonance imaging-based grading systems. We analyzed relationships between radiological grades of CDD and clinical symptoms along with demographic data. RESULTS: One hundred thirteen patients [mean age 44.78, 78 (69%) females] were finally included. CDD occurred most at the C5-C6 level, with 56.93% of higher grade III from Miyazaki. The grades of Miyazaki (P < 0.05) and the scores of Nakashima (P < 0.05) were positively correlated with the duration of symptoms, and the severity of the CDD increased with aging (P < 0.01). Moreover, we correlated patients' JOA scores with the current scoring and grading systems, especially the grades of Miyazaki (P < 0.01) and the scores of Nakashima (P < 0.01). CONCLUSION: Increasing grades of CDD paralleled decreasing JOA scores in the population studied.

Silencing of circular RNA ANRIL attenuates oxygen-glucose deprivation and reoxygenation-induced injury in human brain microvascular endothelial cells by sponging miR-622.

BACKGROUND: Circular RNA (circRNA) is highly expressed in the brain tissue, but its molecular mechanism in cerebral ischemia-reperfusion remains unclear. Here, we explored the role and underlying mechanisms of circRNA antisense non-coding RNA in the INK4 locus (circ_ANRIL) in oxygen-glucose deprivation and reoxygenation (OGD/R)-induced cell injury. RESULTS: The expression of circ_ANRIL in OGD/R-induced human brain microvascular endothelial cells (HBMECs) was significantly up-regulated, while that of miR-622 was significantly down-regulated. Overexpression of circ_ANRIL significantly inhibited the proliferation of OGD/R-induced HBMECs and aggravated OGD/R-induced cell apoptosis. Moreover, circ_ANRIL overexpression further increased the secretion of interleukin (IL)-1ß, IL-6, tumor necrosis factor-α, and monocyte chemoattractant protein-1 in OGD/R-treated HBMECs. The results of bioinformatics analysis and luciferase reporter assay indicated that circ_ANRIL served as an miR-622 sponge to negatively regulate the expression of miR-622 in OGD/R-treated HBMECs. Additionally, circ_ANRIL silencing exerted anti-apoptotic and anti-inflammatory effects by positively regulating the expression of miR-622. Furthermore, inhibition of OGD/R-induced activation of the nuclear factor (NF)-κB pathway by circ_ANRIL silencing was significantly reversed by treatment with miR-622 inhibitor. CONCLUSIONS: Knockdown of circ_ANRIL improved OGD/R-induced cell damage, apoptosis, and inflammatory responses by inhibiting the NF-κB pathway through sponging miR-622.

Silencing of circular RNA ANRIL attenuates oxygen-glucose deprivation and reoxygenation-induced injury in human brain microvascular endothelial cells by sponging miR-622

BACKGROUND: Circular RNA (circRNA) is highly expressed in the brain tissue, but its molecular mechanism in cerebral ischemia-reperfusion remains unclear. Here, we explored the role and underlying mechanisms of circRNA antisense non-coding RNA in the INK4 locus (circ_ANRIL) in oxygen-glucose deprivation and reoxygenation (OGD/R)-induced cell injury. RESULTS: The expression of circ_ANRIL in OGD/R-induced human brain microvascular endothelial cells (HBMECs) was significantly up-regulated, while that of miR-622 was significantly down-regulated. Overexpression of circ_ANRIL significantly inhibited the proliferation of OGD/R-induced HBMECs and aggravated OGD/R-induced cell apoptosis. Moreover, circ_ANRIL overexpression further increased the secretion of interleukin (IL)-1ß, IL-6, tumor necrosis factor-a, and monocyte chemoattractant protein-1 in OGD/R-treated HBMECs. The results of bioinformatics analysis and luciferase reporter assay indicated that circ_ANRIL served as an miR-622 sponge to negatively regulate the expression of miR-622 in OGD/R-treated HBMECs. Additionally, circ_ANRIL silencing exerted anti-apoptotic and anti-inflammatory effects by positively regulating the expression of miR-622. Furthermore, inhibition of OGD/R-induced activation of the nuclear factor (NF)-kB pathway by circ_ANRIL silencing was significantly reversed by treatment with miR-622 inhibitor. CONCLUSIONS: Knockdown of circ_ANRIL improved OGD/R-induced cell damage, apoptosis, and inflammatory responses by inhibiting the NF-κB pathway through sponging miR-622.

Lycopsamine Exerts Protective Effects and Improves Functional Outcome After Spinal Cord Injury in Rats by Suppressing Cell Death.

BACKGROUND Spinal cord injury (SCI) is an injury-triggered event that is associated with permanent neurologic deficit. The deficit instigated by SCI leads to medical co-morbidity, not only affecting sensory and motor capabilities, but also having an impact on the physiological and economic condition of the patient. Against this backdrop, the present study was carried out to investigate the effect of lycopsamine, a plant-derived alkaloid in SCI rats. MATERIAL AND METHODS The traumatic SCI injury in rats was created using a force-calibrated weight-drop device. The Basso-Beattie-Bresnahan (BBB) locomotor rating scale was used to investigate the functional consequences of SCI. DAPI (4',6-diamidino-2-phenylindole) and Tunnel staining were used to detect apoptosis. Western blot and qRT-PCR was used to examine the protein and gene expressions, respectively. RESULTS The results revealed that lycopsamine significantly (p<0.01) improved locomotory function in SCI rats. Lycopsamine also significantly (p<0.01) decreased the lesion area of the SCI rats. Investigation of the effect of lycopsamine on cell death following SCI revealed that lycopsamine reduces apoptotic cell death following SCI. The lycopsamine-induced reduction in apoptosis was allied with downregulation of calpain, cleaved caspase 3 and 9, and Bax. However, the expression of BCl-2 was significantly upregulated. Furthermore, lycopsamine significantly (p<0.01) upregulated the expression of interleukin-10 (IL-10) and decreased the expression of tumor necrosis factor-α (TNF-α). CONCLUSIONS Lycopsamine exerts protective effects in PCI rats by improving functional recovery and suppressing apoptosis.