Effect of hyperbaric oxygen on MMP9/2 expression and motor function in rats with spinal cord injury.
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To study the effect of hyperbaric oxygen intervention on the microenvironment of nerve regeneration after spinal cord injury modeling and to explore the possible mechanism of nerve regeneration and functional recovery in rats with spinal cord injury. In 98 adult female SD rats, 90 successful models were obtained, which were divided into sham group, spinal cord injury group and hyperbaric oxygen group using randomized block method, 30/group. Spinal cord injury rat model was established in accordance with the modified Allen method. Motor function was assessed at the time points of before modeling, one day, three days, one week, two weeks, three weeks and four weeks after modeling respectively by BBB rating, inclined plane test and improved Tarlov score. At 3 days after modeling, apoptosis of neuronal cells in spinal cord injury region in experimental group was detected by TUNEL method; gene and protein expression of MMP9/2 in spinal cord injury and surrounding tissues was detected by RT-PCR and Western blot assay. At 4 weeks after modeling, histopathological morphological changes in spinal cord injury were observed by HE staining; fluorogold retrograde tracing was used to observe the regeneration and distribution of spinal cord nerve fibers and axon regeneration was observed by TEM. The three motor function scores in hyperbaric oxygen group at each time point after two weeks of treatment were significantly increased compared with spinal cord injury group (P < 0.05). At 3 d after modeling, apoptosis index in hyperbaric oxygen group were significantly lower than those in spinal cord injury group (P < 0.05). At 72 h after modeling, compared with spinal cord injury group, MMP9/2 gene and protein expression in hyperbaric oxygen group was significantly lower (P < 0.05). At four weeks after modeling, fluorogold positive nerve fibers were the most sham group, followed by hyperbaric oxygen group and spinal cord injury group in order; the differences among the groups were statistically significant (P < 0.05). Under TEM, newborn unmyelinated and myelinated nerve fibers could be observed in the middle cross-section in the sham group and hyperbaric oxygen group; unmyelinated and myelinated nerve fibers in hyperbaric oxygen group were more than those in spinal cord injury group. Hyperbaric oxygen therapy played a protective effect on spinal cord injury through reducing apoptosis of neuronal cells and expression of MMP9/2 gene and protein in rats with spinal cord injury.Cite
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This article has been retracted, and the online PDF has been watermarked “RETRACTED”. A retraction notice is available at DOI: 10.3233/RNN-239001.
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Objective:To investigate the effect of edaravone on neuroprotection after spinal cord injury in rats. Method:Thirty male Sprague-Dewley rats were randomly assigned to two groups: Control group and experiment group. A standardized model of spinal cord injury was established by the modified Allen′s crush method. The malonyldialdehyde production of spinal cord homogenate was measured by using the thiobarbituric acid test at 2h after injury. Function status was assessed weekly using inclined plane test and the Basso-Beattle-Bresnahan(BBB) locomotor rating scores for 6 weeks. After which the animals were killed for histologic studies, the spared spinal cord area was calculated.Result: After 2 hours, the malonyldialdehyde production of spinal cord homogenate was less in the experiment group than in the control group. There was significant differrence between the two groups. Six weeks after injury, edaravone-treated rats showed significantly higher angle of incline plane test and BBB motor score and larger spared spinal cord area than the control rats. There was significant differrence between the two groups.Conclusion:Edaravone can inhibit posttraumatic lipid peroxide formation,preserve more spinal cord tissue,so that it can enhance nerve functional recovery.
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Objective To study the apoptosis of the neural cells and the changes of caspase-3,AIF′s expression after acute spinal cord injury in rats.Methods The spinal cord injury of the healthy adult SD rats(78)were induced with Nystrom’s way by the moderate compression at the level of T8 and T9 spinal cord.HE method was used to detect the pathologic change of spinal cord.The expression of caspase-3 and AIF was detected by immunohistochemical study.Besides,by using the DUTP nick and labeling(TUNEL)methods which was mediated by terminal deoxynucleotidyl transferase to detect the level of the apoptosis of neural cells.Results There was less expression of AIF,caspase-3 and TUNEL-positive cells in normal and sham operated spinal cord as detected by immunohistochemical study.The number of positive cells of AIF increased clearly 1 day and then reached a peak,but it was rarely seen 5 days after spinal injury.The expression of caspase-3 increased obviously 8 hours after spinal injury,then reached a peak 3 days after spinal injury,but it decreased 7 days after spinal injury.The number of positive cells of TUNEL also increased obviously 8 hours after spinal injury,and then reached a peak on 3 day,and also decreased 7 days after spinal injury.Conclusion There is apoptosis of the neural cells after acute spinal cord injury,and AIF,caspase-3 may be involved in the regulation of the apoptosis of neural cells after acute spinal cord injury.
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Objective To study the effect of electric acupuncture on apoptosis in spinal cord injury. Methods The rats were immediately treated in electric acupuncture after spinal cord injury(T10) by Allen's weight drop (50 g cm force) technique and killed at 6h and 24h after operation. The apoptosis of spinal slice was examined by the method of the terminal deoxynucleotidal transferase mediated dUTP biotin nick end labeling(TUNEL) reaction, the TUNEL positive cells were quantitatively analyzed by computer image analysis system. Result The number of TUNEL positive cells reduced significantly in spinal cord injured rats treated by electric acupuncture. Conclusion Electric acupuncture may prevent the progress of the second spinal cord injury by inhibits the apoptotic neuronal death after spinal cord injury.
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Objective: To observe the changes in the expression of apoptosis regulating gene Bcl-2 and Bax at different time points after acute spinal cord injury.Methods:We randomly divided 56 Wistar rats into 7 groups.we made six groups of the 7 groups as acute spinal cord injury model,the other group was used as control.We evaluated motor capacity at 0h,4h,8h,24h,48h and 72h after injury.The spinal cord was taken and after the HE staining and TUNEL staining,the immunohisto-chemistry methods were used to study the expression of Bcl-2 and Bax.Results:After acute spinal cord injury,the motor capacity decreased.TUNEL-positive cells were found at 4h after injury,with a maximum presence at 8h after injury.At 24h after injury,the positive expression of Bcl-2 was maximal,and the positive expression of Bax was maximal at 8h after injury.Conclusion:In addition to necrosis,apoptosis phenomenon presents in rats spinal cord injury.The proportion of Bcl-2 and Bax in cells may influence upon apoptosis and pathological processes after spinal cord injury.
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To investigate the effects of curcumin on motor function, and to explore the neuroprotective mechanism of curcumin after the spinal cord injury in rats. The study will theoretical and experimental evidence for curcumin's clinical treatment.HI-0400 spinal cord impactor was used to prepare animal models of acute of spinal cord injury. One hundred and five clean and healthy rats were randomly divide into three groups:sham operation group (Sham) spinal cord injury group (SCI) and curcumin group (SCI+CUR). Intragastric administration was administrated after 30min of the spinal cord injury model, after 1 time a day, until the death. SCI+CUR group was intragastric administration with curcumin (100 mg/kg) of 0.5% carboxymethyl cellulose sodium, and Sham and SCI group were treated with the same dose of 0.5% carboxymethyl cellulose sodium. The motor function recovery of 3,7,14,21 and 28 days after spinal cord injury were evaluated by basso,beatlie,bresnahan (BBB) score. The spinal cord tissue and blood samples were collected at postoperative 12 h, 1 d, 3 d and 7 d respectively, NF-kappa B was detected by immunofluorescence, Bcl-2, Bax and Caspase-3 were detected by immunohistochemistry. The expression of Bcl-2 and Bax was detected by Elisa.The statistic difference of BBB score between SCI group and CUR group in 3 day was not statistically significant. It was found that the 7,14,21 and 28 days BBB score in CUR group were statistically significant higher than that in SCI group(P<0.05).The expression of inflammatory factor NF-kappa B appeared in 12 h after spinal cord injury, 1 day peaked and 3 days decreased. In SCI+CUR group, the expression of NF-kappa B at each time point was similar to the SCI group, and there was a difference between group SCI+CUR and SCI group in 1day.There was no obvious staining of Bax and Bcl-2 in Sham group. The staining of Caspase-3 and Bax in SCI+CUR group was significantly weaker than that in SCI group, while Bcl-2 was stronger.Curcumin can promote the recovery of hindlimb motor function after spinal cord injury in rats.The mechanism is through inhibition of NF-K B to prevent inflammation; And inhibition the expression of Bax and Caspase-3, and promotion the expression of Bcl-2 to prevent apoptosis, so as to accelerate the recovery of motor function in the rats after spinal cord injury.
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This work examines whether microglia-conditioned medium (MCM) is beneficial in stressed spinal cord cells or tissues. MCM was separated into two fractions by 50 kDa molecular cut-off centrifugation. MCM not only promoted survival of neuronal and oligodendroglial cells but effectively reduced LPS stimulation in spinal cord cultures. We further utilized the NYU weight-drop device to induce contusive spinal cord injury (SCI) in rats. Immediately after dropping the impactor from a height of 25 mm onto thoracic spinal segment, MCM was intrathecally administered. At 6 weeks post-injury, SCI rats receiving MCM > 50 kDa treatment showed significant hind-limb improvement over MCM 50 kDa, of microglia was neuroprotective against spinal cord injury.
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Objective To study the neuroprotective effect of high-dose methylprednisolone in prophylaxis in rat acute spinal cord injury. Methods The rats were randomly divided into three groups:Control groups,acute spinal cord injury groups,administration of methylprednisolone in prophylaxis. Allen's weight drop model of acute spinal cord injury was prepared and to study the ratio of Tarlov's motor scales,ratio of Molt's inclined plane scales,pathological and ultrastructural changes of spinal cord,neurofilament and glial fibrillary acidic protein at 24- and 72-hour after ASCI,respectively. Results The pathological and ultrastructural changes of spinal cord were significantly improved in MP groups. The neurological function of rats in MP groups was significantly improved at 72-hour after ASCI. The expression of NF significantly increased and the expression of GFAP significantly decreased in MP groups. Conclusion There is neuroprotective effect of high-dose methylprednisolone in prophylaxis in rat acute spinal cord injury.
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Objective:To investigate the neuroprotection and mechanisms of 17 beta-estradiol after spinal cord injury(SCI) in rats.Method:Rat model of SCI was established with a modified Allen′s method.The experimental rats were randomly divided into two groups:group A,phosphate buffer saline(PBS) group and group B,17 beta-estradiol experimental group.Each group consisted of 42 rats.Rats in group B received 4.0 mg/kg of 17 beta-estradiol,which was dissolved in PBS at 15min and 24h post-injury,while rats in group A were treated with an equal volume of PBS at the same time point.The neurofunction of spinal cord was evaluated by modified Tarlov score and Rivlin platform test at 7d,14d,21d and 28d after injury respectively.The animals were sacrificed at 6h,24h,3d,7d,14d and 28d respectively after injury.The lesion areas of the spinal cord were dissected for morphological studies by hematoxylin and eosin staining.Cell apoptosis was examined using the TUNEL assay and the expression of caspase-3 and Bcl-2 were detected using immunohistochemistry method.Result:From the 14th day after treatment,the neurofunction of the spinal cord was significantly better in group B than that in group A(P0.01).Apoptotic cells were noted in rats after SCI,and peaked at 3rd day after SCI,which was consistent with the expression of caspase-3.The apoptotic rate in group B decreased significantly as compared with that in group A at the time points of 24h,3d and 7d(P0.01 or P0.05).In group B,the expression of caspase-3 decreased significantly,while Bcl-2 significantly improved as compared with that in group A at the time points of 24h,3d,7d,14d and 28d after SCI(P0.01 or P0.05).Conclusion:17 beta-estradiol can reduce the numbers of apoptotic cells and promote the nerve function recovery after SCI.
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