1.Mechanism of Jisuishang Formula in cervical spondylotic myelopathy:Regulation of neuronal injury via the Wnt/β-catenin signaling pathway
Hanli YANG ; Chunzhi LIU ; Ming SHI ; Minggao HU ; Xianzhong BU ; Yuanming ZHONG ; Wei XU
The Journal of Practical Medicine 2025;41(10):1487-1495
Objective To investigate the mechanism of Jisuishang Formula on cervical myelopathy based on Wnt/β-catenin signaling pathway.Methods Thirty-six adult male SD rats were randomly divided into sham operation group,model group,positive control group(TAK-715,50 mg/kg),Jisuishang Formula low(9.7 g/kg),medium(19.4 g/kg)and high(38.8 g/kg)dose groups,with 6 rats in each group for 4 weeks.The BBB score and inclined plate test were observed at 1,2 and 4 weeks after surgery.HE and Nissl staining were used to observe the histopathology and neuronal condition of the spinal cord.Immunofluorescence was used to detect the protein expres-sions of BDNF,β-catenin,Bax and Bcl-2.Western blot and qRT-PCR were used to detect the expression of Wnt/β-catenin signaling pathway-related proteins and mRNAs.Results Compared with the sham group,the BBB score and inclined plate test score were significantly decreased(P<0.05),the expressions of BDNF,β-catenin and Bcl-2 decreased(P<0.05),the expression of Bax increased(P<0.05),the expressions of β-catenin,LRP-6 and p-GSK-3βdecreased(P<0.05),and the expressions of Caspase-3 and Caspase-9 increased(P<0.05).Compared with the model group,the BBB score and inclined plate test score were significantly increased in the high-dose Jisuishang Formula group(P<0.05),the expressions of BDNF,β-catenin and Bcl-2 increased(P<0.05),the expression of Bax decreased(P<0.05),the expressions of β-catenin,LRP-6 and p-GSK-3βincreased(P<0.05),and the expressions of Caspase-3 and Caspase-9 decreased(P<0.05).Conclusion Jisuishang Formula prescription can inhibit neuronal apoptosis,improve spinal cord microenvironment,and promote neurological function recovery by activating the Wnt/β-catenin signaling pathway.
2.Mechanism of Jisuishang Formula in cervical spondylotic myelopathy:Regulation of neuronal injury via the Wnt/β-catenin signaling pathway
Hanli YANG ; Chunzhi LIU ; Ming SHI ; Minggao HU ; Xianzhong BU ; Yuanming ZHONG ; Wei XU
The Journal of Practical Medicine 2025;41(10):1487-1495
Objective To investigate the mechanism of Jisuishang Formula on cervical myelopathy based on Wnt/β-catenin signaling pathway.Methods Thirty-six adult male SD rats were randomly divided into sham operation group,model group,positive control group(TAK-715,50 mg/kg),Jisuishang Formula low(9.7 g/kg),medium(19.4 g/kg)and high(38.8 g/kg)dose groups,with 6 rats in each group for 4 weeks.The BBB score and inclined plate test were observed at 1,2 and 4 weeks after surgery.HE and Nissl staining were used to observe the histopathology and neuronal condition of the spinal cord.Immunofluorescence was used to detect the protein expres-sions of BDNF,β-catenin,Bax and Bcl-2.Western blot and qRT-PCR were used to detect the expression of Wnt/β-catenin signaling pathway-related proteins and mRNAs.Results Compared with the sham group,the BBB score and inclined plate test score were significantly decreased(P<0.05),the expressions of BDNF,β-catenin and Bcl-2 decreased(P<0.05),the expression of Bax increased(P<0.05),the expressions of β-catenin,LRP-6 and p-GSK-3βdecreased(P<0.05),and the expressions of Caspase-3 and Caspase-9 increased(P<0.05).Compared with the model group,the BBB score and inclined plate test score were significantly increased in the high-dose Jisuishang Formula group(P<0.05),the expressions of BDNF,β-catenin and Bcl-2 increased(P<0.05),the expression of Bax decreased(P<0.05),the expressions of β-catenin,LRP-6 and p-GSK-3βincreased(P<0.05),and the expressions of Caspase-3 and Caspase-9 decreased(P<0.05).Conclusion Jisuishang Formula prescription can inhibit neuronal apoptosis,improve spinal cord microenvironment,and promote neurological function recovery by activating the Wnt/β-catenin signaling pathway.
3.Effects of enriched rehabilitative training on the expression of MAP-2 and SYN after the reperfusion of ischemic brain injury
Cheng JIANG ; Weijing LIAO ; Wantong YANG ; Lanqing MENG ; Qin ZHOU ; Xiaoqin HU ; Minggao CHENG
Chinese Journal of Physical Medicine and Rehabilitation 2008;30(11):750-755
Objective To study the effects of enriched rehabilitative training on the expression of microtu-bule associated protein 2 (MAP-2) and synaptophysin (SYN), and to explore its relationship with brain plasticity. Methods Seventy-seven male Wistar rats weighing 160 to 200 g were randomly divided into an ischemia + enriched rehabilitation group (IE, n=36), an ischemia + standard rehabilitation group(IS, n=8), a sham ischemia + en-riched rehabilitation group (SE, n=21) and a sham ischemia + standard rehabilitation group (SS, n=12). Rats in the ischemia groups had their middle cerebral artery sutured for two hours before reperfusion, while those in the sham groups had a similar operation without occlusion. The enriched groups were given enriched rehabilitative train-ing, while the standard groups were left without any training. Behavioral tests, including the acrobatic performance, were administered once daily 2 days after operation, and SP staining of MAP2 and SYN were used to observe the func-tional recovery and brain plasticity changes among the groups at 1,7, 14, 21 and 28 days after the operations. Re-sults Acrobatic performance times reduced gradually. Bederson scores were significantly better in the IE than in the IS group by the 28th day after the operation). There was no significant difference between IE and IS groups in a foot fault test). The expression of MAP-2 and SYN around the infarct and in the hippocampus decreased significantly at first), then recovered gradually. The expression of MAP-2 and SYN in the IE group was significantly higher than that in the IS group at various time points of observation). Conclusion Enriched rehabilitative training can improve functional recovery and the expression of MAP-2 and SYN after brain ischemia, and the functional enhancement may attribute to the brain plasticity.

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