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【Objective】 To report the early clinical effects and surgical complications of endoscopic spinal fusion technology （Endo-LIF） in the treatment of degenerative lumbar disease. 【Methods】 The clinical data of 31 patients with degenerative lumbar spine disease treated with Endo-LIF from June 2019 to May 2021 were retrospectively analyzed. All the 31 patients underwent endoscopic spinal fusion therapy. We recorded the operation time， hospital stay duration， postoperative complications， visual analogue scale for pain （VAS）， oswestry dysfunction Index （ODI） and low back pain in the Chinese Orthopaedic Association Spine Group Surgery scoring standards before operation， immediately after operation， and the last follow-up to evaluate clinical efficacy. 【Results】 The operation time of the 31 patients was （134.80±34.98） min， the intraoperative blood loss was （100.13±18.49） mL， the hospital stay was （6.65±0.17） days， and the follow-up time was 6 to 18 （14±2.3） months. One patient had hematoma compression after surgery； he had incision made immediately to clear the hematoma and healed after bed rest. Two patients developed spinal hypertension and healed after bed rest. All the patients had no symptoms of nerve injury after operation， and the clinical symptoms were significantly relieved. We compared the perioperative VAS score and ODI index of all the patients， which were lower immediately after operation and at the last follow-up than those before the operation （P<0.05）， and the difference was statistically significant. 【Conclusion】 Endo-LIF technology has good short-term clinical effects and the advantages of milder trauma， less blood loss， and quick recovery after surgery. It is a safe and minimally invasive lumbar fusion surgery.
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@#Objective To observe the effects of different dosages of ginsenoside Rb1 preconditioning on spinal cord ischemia-reperfusion injury in rats, and the possible mechanism. Methods Sprague-Dawley rats were randomly divided into sham group (n=12), model group (n=12), and 10 mg/kg (D10, n=12), 20 mg/kg (D20, n=12), 40 mg/kg (D40, n=12) and 80 mg/kg (D80, n=12) drug groups. Spinal cord ischemia for ten minutes and reperfusion model was established, and the drug groups were injected ginsenoside Rb1 intraperitoneally in their dosages 30 minutes before modeling. They were assessed with BBB score 48 hours after reperfusion, and then were sacrificed for HE staining, TUNEL staining and immunohistochemistry staining of survivin.Results The BBB score was more in the drug groups than in the model group (P<0.05), and was the most in D40 and D80 groups. The expression of survivin was more in the drug groups than in the model group (P<0.05), and was the most in D40 and D80 groups. The apoptosis of neurons was less in the drug groups than in the model group (P<0.05), and was the least in D40 and D80 groups.Conclusion The ginsenoside Rb1 could promote the expression of survivin, inhibit apoptosis of neurons, to protect the neural function, in dose-dependent manner somehow.
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Objective To investigate the effect of ginsenoside Rg1 on apoptosis after spinal cord ischemia-reperfusion injury (SCII) in rats. Methods Forty-eight adult Sprague-Dawley rats were randomly divided into sham group (n=8), ischemia group (n=8), ischemia-reper-fusion group (n=16) and drug group (n=16). Fogarty catheter was put in the thoracic aorta of the rats and the blood flow wasn't blocked in the sham group. The rats in the ischemia group were sacrificed 30 minutes after spinal cord ischemia. The drug group was injected with gin-senoside Rg1 30 mg/kg 30 minutes before and after SCII. The same volume of normal saline was injected in the ischemia-reperfusion group at the same time. The expression of Bcl-2 and survivin was detected with immunohistochemistry at six hours, 24 hours after reperfusion in the ischemia-reperfusion group and drug group, 30 minutes after ischemia in the ischemia group and in the sham group. The change of cells was observed in each group with HE staining. Results The cells were damaged in the ischemia group, the ischemia-reperfusion group and the drug group, in which the drug group was better than the other groups. The expression of survivin and Bcl-2 was higher in the ischemia group, the ischemia-reperfusion group and the drug group than in the sham group (t>3.896, P6.693, P<0.001). Conclusion Ginsenoside Rg1 can reduce the neurons damage and increase the expression of the Bcl-2 and survivin, that inhibit cells apoptosis after SCII in rats.
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Objective To investigate the effects of erigeron breviscapus (Vant.) Hand-Mazz (erigeron breviscapus) pretreatment on pathology and oxyradical level in the spinal cord after ischemia-reperfusion (I/R) injury in rabbits. Methods A total of 40 New Zealand white rabbits were randomly divided into three groups: sham-operation group with 10 rabbits treated with only abdominal aorta exposure without occlusion, control group with 15 rabbits that underwent ischemia for 50 minutes and treated with matched saline, and experimental group with 15 rabbits that underwent ischemia for 50 minutes and treated with erigeron breviscapus (9mg/kg) injection before ischemia. Malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in the spinal cord were examined at 6 and 24 hours after I/R, respectively. The morphological changes and the number of the spinal cord anterior horn motor neurons were observed and counted under the light microscope and electron microscope, respectively. Results The level of MDA was markedly decreased and SOD activity was increased in the experimental group compared with those in the control group (P<0.01). Compared with that in the control group, the number of motor neurons in the experimental group significantly increased at 24h after I/R (P<0.01) and the morphous of the motor neurons improved. Conclusion Erigeron breviscapus can reduce oxyradical production and the apoptosis of nerve cells, and protect nerve tissue structure and function after spinal cord I/R.
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Objective: To investigate the mechanisms of mitochondrial apoptosis in spinal cord ischemia-reperfusion injury and the effects of Herba Erigerontis Breviscapi Injection preconditioning intervention. Methods: Sixty Japanese rabbits were divided into sham-operated group, ischemia group, ischemia-reperfusion group (1, 6, 24 and 48 h), and Herba Erigerontis Breviscapi Injection group (1, 6, 24 and 48 h). Clamping the abdominal aorta was used to construct the rabbit model of spinal cord ischemia-reperfusion injury. The rabbits in the ischemia-reperfusion group and the Herba Erigerontis Breviscapi Injection group underwent reperfusion for 1, 6, 24, 48 h respectively after fifty-minute ischemia. The rabbits in the Herba Erigerontis Breviscapi Injection group were administered with Herba Erigerontis Breviscapi Injection at 9 mg/kg 30 minutes before ischemia. Rate of apoptotic cells was measured by flow cytometry; contents of caspase-9 and apoptosis-inducing factor (AIF) in cytoplasm and serum were measured by enzyme-linked immunosorbent assay. Results: Compared with the sham-operated group and the ischemia group, the rates of apoptotic cells, the contents of caspase-9 and AIF in cytoplasm were increased at all time points after reperfusion, and the contents of caspase-9 and AIF in serum were decreased after 1 h and 6 h reperfusion, and increased after 24 h and 48 h reperfusion in the ischemia-reperfusion group. Herba Erigerontis Breviscapi Injection intervention could decrease the rate of apoptotic cells and the contents of caspase-9 and AIF in cytoplasm and serum as compared with those in the ischemia-reperfusion group, and the effects appeared after 1 h reperfusion. Conclusion: The apoptosis of nerve cells after spinal cord ischemia-reperfusion is related to the mitochondrial pathways. Herba Erigerontis Breviscapi Injection can inhibit nerve cell apoptosis by decreasing the contents of caspase-9 and AIF in cytoplasm and serum.
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@# Objective To observe the effect of aprotinin preconditioning on nitric oxide (NO), nitric oxide synthase (NOS) and oxyradical during spinal cord ischemia-reperfusion injury in rabbits.Methods 21 rabbits were randomly divided into the aprotinin treatment group (8 rabbits), control group (8 rabbits) and sham operative group (5 rabbits). The infrarenal segment in abdominal aorta was clamped for 60 min to construct the model of lumbosacral spinal cord ischemia in rabbits. Reperfusion was followed and kept on for 24 h until the blood flow regained normal. In the treatment group, aprotinin was given at 3×107 IU/kg as a short time intravenous injection for 10 min before ischemia, and then was drilled with micro pump by 1×107 IU/kg/h. Normal saline was used in the control group, the ischemia-reperfusion duration between aprotinin treatment group and control group remained same. The sham operative group was only exposured abdominal aorta and not clamped. The rabbits were killed before ischemia and 8 h, 24 h after ischemia-reperfusion, lumbar segment was harvested to detect content of NO, malondialdehyde (MDA), induced nitric oxide synthase (iNOS) and superoxide dismutase (SOD) of spinal cord.Results 8 h after spinal cord ischemia-reperfusion, compared with the control group, the content of NO, MDA and the activity of iNOS were less, and the activity of SOD was more in the aprotinin treatment group ( P<0.05).Conclusion Aprotinin pretreatment can reduce the content of NO, MDA and descend the activity of NOS. Moreover aprotinin pretreatment can ascend the activity of SOD and improve apoptosis of nerve cell.
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@#Objective To observe the effect of pretreatment of aprotinin on nitric oxide (NO) and nitric oxide synthase (NOS) contents after ischemia-reperfusion injury of spinal cord in rabbits.Methods 45 rabbits were randomly divided into aprotinin treatment group (group A), normal saline control group (group B) and pseudo-surgical operation group (group C) with 15 rabbits in each group. The infrarenal segment in abdominal aorta was clamped for 60 min to construct the model of lumbosacral spinal cord ischemia in rabbits. Reperfusion was followed and kept on for 24 h until the blood flow regained normal. Aprotinin was given 3×107 IU/kg as a short time intravenous injection for 10 min before ischemia, and then was drilled with micro pump by 1×107 IU/kg/h. Normal saline was used in group B, the ischemia-reperfusion duration between group A and group B remained same. The group C was only exposured abdominal aorta and not clamped. The rabbits were killed before ischemia and at 8 h, 24 h after ischemia-reperfusion, lumbar segment spinal cords were harvested to detect contents of NO and NOS of spinal cord.Results After 8 h of ischemia-reperfusion,the contents of NO, total NOS (TNOS), and induced NOS (iNOS) in group A and group B were more than that before ischemia (P＜0.05). After 8 h of ischemia-reperfusion, there was a significant difference in the contents of NO, TNOS, iNOS between group A and group B (P＜0.05～0.01). After 24 h of ischemia-reperfusion, there was a significant difference too between group A and group B (P＜0.01). After 8 h and 24 h ischemia-reperfusion, the contents of NO, TNOS, iNOS in group A and group B were more than that in group C (P＜0.01).Conclusion During the ischemia-reperfusion, more NO produced is an important factor of spinal cord injury. Aprotinin can decrease the contents of NO and ischemia-reperfusion injury to spinal cord of rabbits.