Lee, SM Yune, TY Kim, SJ Park, DW Lee, YK Kim, YC Oh, YJ Markelonis, GJ Oh, TH 2024-01-21T08:09:00Z 2024-01-21T08:09:00Z 2021-09-03 2003-10 0897-7151 https://pubs.kist.re.kr/handle/201004/138192 We examined the effects of minocycline, an anti-inflammatory drug, on functional recovery following spinal cord injury (SCI). Rats received a mild, weight-drop contusion injury to the spinal cord and were treated with the vehicle or minocycline at a dose of 90 mg/kg immediately after SCI and then twice at a dose of 45 mg/kg every 12 h. Injecting minocycline after SCI improved hind limb motor function as determined by the Basso-Beattie-Bresnahan (BBB) locomotor open field behavioral rating test. Twenty four to 38 days after SCI, BBB scores were significantly higher in minocycline-treated rats as compared with those in vehicle-treated rats. Morphological analysis showed that lesion size increased progressively in both vehicle-treated and minocycline-treated spinal cords. However, in response to treatment with minocycline, the lesion size was significantly reduced at 21-38 days after SCI when compared to the vehicle control. Minocycline treatment significantly reduced the number of terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL)-positive cells 24 h after SCI as compared to that of the vehicle control. DNA gel electrophoresis also revealed a marked decrease in DNA laddering in response to treatment with minocycline. In addition, minocycline treatment significantly reduced the specific caspase-3 activity after SCI as compared to that of vehicle control. Furthermore, RT-PCR analyses revealed that minocycline treatment increased expression of interleukin-10 mRNA but decreased tumor necrosis factor-alpha expression. These data suggest that, after SCI, minocycline treatment modulated expression of cytokines, attenuated cell death and the size of lesions, and improved functional recovery in the injured rat. This approach may provide a therapeutic intervention enabling us to reduce cell death and improve functional recovery after SCI. English MARY ANN LIEBERT, INC TUMOR-NECROSIS-FACTOR FACTOR-ALPHA MESSENGER-RNA CONTROLLED TRIAL GLIAL APOPTOSIS ACTIVATION CONTUSION METHYLPREDNISOLONE INFLAMMATION EXPRESSION Minocycline reduces cell death and improves functional recovery after traumatic spinal cord injury in the rat Article 10.1089/089771503770195867 1 JOURNAL OF NEUROTRAUMA, v.20, no.10, pp.1017 - 1027 JOURNAL OF NEUROTRAUMA 20 10 1017 1027 scie scopus 000186072300010 2-s2.0-0142025464 Critical Care Medicine Clinical Neurology Neurosciences General & Internal Medicine Neurosciences & Neurology Article TUMOR-NECROSIS-FACTOR FACTOR-ALPHA MESSENGER-RNA CONTROLLED TRIAL GLIAL APOPTOSIS ACTIVATION CONTUSION METHYLPREDNISOLONE INFLAMMATION EXPRESSION apoptosis BBB score caspase-3 DNA laddering functional recovery IL-10 inflammation lesion area minocycline spinal cord injury TUNEL