Effects of decompression joint Governor Ves(3)

Effects of decompression combined with EA on platelet-activating factor contents in injured tissues of rats with acute upper cervical SCI

Figure 1 Establishment of a rat model of acute upper cervical spinal cord injury.(A) Exposure of the atlanto-occipital and atlanto-axial space; (B) insertion of balloon catheter (arrow) into the space; (C) balloon catheter compression system; (D) completion of the model.

Figure 3 Comparison of tissue platelet-activating factor content in the groups compressed for 12 and 48 data are expressed as the mean ±SD (n= 6 per group). *P＜ 0.05,vs.sham group; #P＜ 0.05,vs. EA group;?P＜ 0.05,vs. MP group (one-way analysis of variance followed by the least significant differencepost hoctest). EA: Electroacupuncture; MP:methylprednisolone; SCI: spinal cord injury.

Figure 2 Treatment by Governor Vessel electroacupuncture.

Figure 4 Comparison of caspase-9 protein expression in the groups compressed for 12 and 48 hours(western blot assay).The caspase-9 expression was lower in the 12-hour and the 48-hour EA groups than in the 12-hour MP and SCI groups, and the 48-hour MP and SCI groups. The caspase-9 expression was lower in the 12-hour and the 48-hour MP groups than in the 12-hour and the 48-hour SCI groups. All data are expressed as the mean ± SD (n= 6 per group). *P＜ 0.05,vs.sham group; #P＜0.05,vs. EA group; ?P＜ 0.05,vs. MP group(one-way analysis of variance followed by the least signi fi cant differencepost hoctest).EA: Electroacupuncture; MP: methylprednisolone; SCI: spinal cord injury.

ELISA results showed that the trends for changes in platelet-activating factor among groups were similar. The platelet-activating factor contents for the groups were as follows: sham group＜ EA group ＜ MP group ＜ SCI group (P＜ 0.05; Figure 3).

Effects of decompression combined with EA on caspase-9 protein expression in injured spinal cord tissues of rats with acute upper cervical SCI

Western blot assay results showed that the trends for changes in caspace-9 expression among groups were similar. The caspase-9 protein expression in the groups were as follows:sham group ＜ EA group ＜ MP group ＜ SCI group (P＜ 0.05;Figure 4).

Discussion

Early decompression has been proven to be more effective in neural functional recovery than delayed decompression following acute SCI. Regarding the pathophysiology, early decompression can more effectively improve neurological function after SCI by inhibiting the expression of tumor necrosis factor α compared with delayed decompression (Xie et al., 2015). Additionally, delayed decompression can exacerbate reperfusion injury and is associated with ongoing enhanced levels of cytokine expression, microglial activation,and astrogliosis (Vidal et al., 2017). Decompression can only remove the insult above the spinal cord. The pathological lesion cannot be completely cured, and thus adjuvant treatment is necessary. In light of the different therapeutic effects of early and delayed decompression, different adjuvant treatments are necessary.

In the traditional Chinese medicine approach, SCI is thought to be strongly associated with stasis of the Governor Vessels. The disturbance of the microcirculation after SCI is an important link between neurological injury, cardiovascular complications, and the change in hemodynamics after SCI (Sezer et al., 2015), which are consistent with stasis of the Governor Vessels in traditional Chinese medicine. Governor Vessel EA can be used at the lesion site to facilitate the recovery of nerve function. This study investigated the effect of early and delayed decompression combined with EA after acute SCI from the standpoint of recovering neural function, improving spinal microenvironment, and inhibiting apoptosis.

In this study, in the groups compressed for 12 hours, BBB scores showed that the recovery of neural function was fast in the EA and MP groups. However, the final recovery of the three groups was similar. For the groups compressed for 48 hours, BBB scores showed that the recovery of neural function was fast and the fi nal recovery was good in the EA and MP groups; moreover, the final recovery was similar among the three groups. Therefore, for decompression at 12 hours, EA and MP treatment can promote the recovery of motor function, but may not make a difference in fi nal functional recovery. For decompression at 48 hours, EA and MP treatment can promote the recovery of motor function and improve the fi nal functional recovery.

Platelet-activating factor is a soluble phospholipid metabolite that can cause the platelet to be activated, released, and aggregated. Platelet-activating factor has been proven to be an important pathological factor for secondary damage after SCI. Once SCI occurs, the platelet-activating factor content will rise rapidly in the SCI tissue, and prompt microvascular thrombosis, vascular endothelial cell damage, increased permeability of blood vessel walls, and blood-spinal cord barrier disruption, thereby altering the microenvironment of the injured spinal cord (Lindsberg et al., 1990; Faden et al., 1992; Xiao et al., 1996). Platelet-activating factor can promote platelet activation by strengthening the expression of adhesion molecule on the surface of platelets. The activation of platelets can combine and activate leukocytes, releasing a large number of oxygen free radicals, interleukins,and tumor necrosis factor-α, with in fl ammatory in fi ltration occurring around the injured spinal cord tissue (Guo et al.,2005), In this study, for the groups compressed for 12 and 48 hours, the change was similar; in other words, platelet-activating factor content was decreased in the EA group compared with the MP and SCI groups. These results confi rm that EA can strongly improve the microenvironment of the injured spinal cord, and the EA group had a better longterm outcome than the MP and SCI groups.

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