Salvianolic acid B activates Wnt/β‑catenin signaling following spinal cord injury
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Abstract:
Neural cell apoptosis serves a key role in spinal cord injury (SCI), which is a threat to human health. The present study aimed to evaluate the neuroprotective mechanism of salvianolic acid B (Sal B) in a spinal cord injury (SCI) rat model. Basso, Beattie, and Bresnahan scores demonstrated that Sal B treatment significantly increased locomotor functional recovery in SCI rats compared with SCI model rats between 3 and 8 weeks. Nissl staining demonstrated that Sal B enhanced motor neuron survival and decreased lesion size after SCI. Reverse transcription-quantitative PCR analysis demonstrated that Sal B treatment significantly enhanced the mRNA levels of lymphoid enhancer biding factor-1 and HNF1 homeobox A. In addition, Sal B treatment enhanced the expression of β-catenin. Western blot analysis determined that Sal B treatment significantly decreased the expression of pro-apoptosis proteins, including Bax, cleaved caspase-3 and -9, in spinal cord tissues after SCI but enhanced the expression of Bcl-2, an anti-apoptotic protein. Furthermore, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining demonstrated that, compared with the SCI group, Sal B treatment decreased the number of TUNEL-positive neurons. In summary, the present study produced novel data demonstrating the neuroprotective effect of Sal B on SCI with the mechanism likely primarily mediated via the Wnt/β-catenin signaling pathway. The present findings may be of potential therapeutic value for future SCI treatments.Keywords:
Terminal deoxynucleotidyl transferase
Nissl body
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ABSTRACT Whether rapamycin has neuroprotective effects in spinal cord injury remains controversial. The present study shows that rapamycin protects neurons from death after spinal cord injury by inhibiting the secondary inflammatory response. The effects of rapamycin were tested using a myeloperoxidase assay, Western blotting, immunohistochemistry, and the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The experimental results showed that after spinal cord injury, rapamycin reduced the numbers of activated microglia and neutrophils in the damage zone, lowered the expression levels of TNF‐α and IL‐1β, reduced the apoptotic cells, and increased the survival of neurons. The above data proved that rapamycin diminishes inflammatory cell activation and proliferation, downregulates the expression of inflammatory factors, reduces the microenvironmental damage effects on neurons in the acute injury phase, and thus promotes the survival of neurons. Therefore, we believe that rapamycin has neuroprotective effects in spinal cord injury.
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Objective: To study the characteristics of neural cells with apoptosis after acute spinal cord injury.Methods:The spinal cord injury of the Wistar rats was induced with Allen's way by a 10g×2.5cm impact on the posterior T_ 8,9 spinal cord.Rats were sacrificed at 1,4,8,24,72 hours and 7,14,21 days after injury(n=6 for each time point).Three segments of every spinal cord were cut for morphological studies,including hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods.Results:TUNEL-positive cells were found in the compression region and neighbor regions after 4h,with a maximum presence at 24h in the compressed segment,and labeled glial cells in white matter reached a peak at 72h.But the labeled cells in the neighboring segments reached a peak at 72h after injury.Both the neural and glial cells in gray matter were expressed TUNEL positive,especially the glial cell.Conclusions:Apoptosis of neural cells is an important morphological change in the secondary lesion period after spinal cord injury.
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Objective:To investigate whether spinal cord decompression is related to neural cell apoptosis after spinal cord injury.Methods:The spinal cord was compressed posteriorly at L1 level using a self-designed compression device for 6,12 h and 24 h,followed by decompression by removal of the screw.Apoptosis and cellular damage were assessed by the staining of HE、Nissl、terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)and immunostaining of caspase-3.Results:Compared with shame-operation group,the number of TUNEL positive cells was significantly higher in the decompression at 6、12、24 h after spinal cord injury,which was consistent with immunoreactive to caspase-3(P0.05).Conclusion:The results indicate that the dynamic change of apoptosis was correlated with duration of spinal compression.Early decompression could reduce neural cell apoptosis following secondary spinal cord injury.
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Spinal decompression
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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 investigate the effect of bcl-xL gene transfection on the expression of Caspase-3 and neuroprotective functionl in rat spinal cord compression injury model.Methods Models of acute spinal cord compression injury at the level of T8,9 were set up.The rats were divided into control group and bcl-xL group.The rats of bcl-xL group were subjected to the intraspinal injection of pSFFV.bcl-xL complexed with liposome.The expression of bcl-xL and Caspase-3 at 1st day,3rn day or 7th day after injection was detected by RT-PCR and immunostaining.The segments of injuried spinal cord were harvested for morphological studies after injury.By using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods,cell apoptosis was detected.Results Compared to control group,the expression of Caspase-3 was significantly decreased (P 0.05) and the number of TUNEL labeling positive cells was less at different time points (P 0.05) in bcl-xL gene transfecting group.Conclusion bcl-xL overexpressed by gene transfecting in injured spinal cord tissue could decrease the post-traumatic apoptosis,which might be correlate with the down-regulation of Caspase-3.
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Objectives: To study the characteristics of neural cells with apoptosis after acute spinal cord injury. Methods: The spinal cord injury of the Wistar rats was induced with Allens way by a 10 g× 2.5 cm impact on the posterior T 8, 9 spinal cord. Rats were sacrificed at 1,4,8,24,72 hours and 7,14,21 days after injury( n =6 for each time point). Three segments of every spinal cord were cut for morphological studies, including hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) methods. Results: TUNEL positive cells were found in the compression region and neighbor regions after 4 h, with a maximum presence at 24 h in the compressed segment, and labeled glial cells in white matter reached a peak at 72 h. But the labeled cells in the neighboring segments reached a peak at 72 h after injury. The TUNEL positive cells were neural and glial cells in gray matter, especially in the latter one. Conclusions: Apoptosis of neural cells is an important morphological change in the secondary lesion period after spinal cord injury.
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In order to study the mechanism of the effect of heparin on apoptosis in carcinoma cells, the nasopharyngeal carcinoma cell line CNE2 was used to identify the effect of heparin on apoptosis associated with the expression of c-myc, bax, bcl-2 proteins by use of Hoechst 33258 staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), agarose gel electrophoresis, and flow cytometry, as well as Western blot analysis. The results showed that heparin induced apoptosis of CNE2 cells including the morphologic changes such as reduction in the volume, and the nuclear chromatin condensation, as well as the “ladder pattern” revealed by agarose gel electrophoresis of DNA in a concentration-dependent manner.The number of TUNEL-positive cells was dramatically increased to 33.6±1.2% from 2.8±0.3% by treat ment with heparin in different concentrations (10～40 kU/L). The apoptotic index was increased to 32.5% from 3.5% by detecting SubG1 peaks on flow cytometry. Western blot analysis showed that levels of bcl-2,bax and c-myc were significantly overexpressed by treatment with the increase of heparin concentrations.These results suggest that heparin induces apoptosis of CNE2 cells, which may be regulated by differential expression of apoptosis-related genes.
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Objective To investigate the effect of interleukin-10 (IL-10) on rat neural cell apop-
tosis after experimental spinal cord injury (SCI). Methods The experimental rats were divided into
three groups: SCI group (group A), IL-10 group (group B) and sham group (no spinal cord injury). The
SCI model was induced using the modified Allen technique and the rats in group B were treated with IL-
10 at 30 min after SCI. The apoptosis and functional recovery of the injured spinal cord were evaluated by
HE staining, TUNEL method and BBB open-field behavioral test respectively at 12 h, 24 h, 48 h, 4 d, 8
d, 16 d and 24 d after SCI. Results Apoptotic cells were noted primarily at 12 h, and peaked at 48 h af-
ter SCI. The apoptotic rate in group B was significantly decreased as compared with that in group A at the
time points of 24 h, 48 h, 4 d after SCI (P 0. 01, or P 0. 05), and the functional recovery was better
in group B than in group A. Conclusion The early adminstration of IL-10 could inhibit apoptosis after
SCI.
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