Inhibition of inflammation and oxidative stress by Angelica dahuricae radix extract decreases apoptotic cell death and improves functional recovery after spinal cord injury

2011 ◽  
Vol 90 (1) ◽  
pp. 243-256 ◽  
Author(s):  
Youn Joo Moon ◽  
Jee Youn Lee ◽  
Myung Sook Oh ◽  
Youngmi Kim Pak ◽  
Kang-Sik Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Functional Recovery ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cord Injury ◽  
And Oxidative Stress

scholarly journals Inhibition of Apoptotic Cell Death by Ghrelin Improves Functional Recovery after Spinal Cord Injury

Endocrinology ◽  
2010 ◽  
Vol 151 (8) ◽  
pp. 3815-3826 ◽  
Author(s):  
Jee Y. Lee ◽  
Hyunju Chung ◽  
Young S. Yoo ◽  
Young J. Oh ◽  
Tae H. Oh ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Functional Recovery ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cord Injury

scholarly journals Changes in Expression of Receptor-Interacting Protein Kinase 1 in Secondary Neural Tissue Damage Following Spinal Cord Injury

2020 ◽  
Vol 15 ◽  
pp. 263310552090640
Author(s):  
Haruo Kanno ◽  
Hiroshi Ozawa ◽  
Kyoichi Handa ◽  
Taishi Murakami ◽  
Eiji Itoi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Tissue Damage ◽  
Time Course ◽  
Apoptotic Cell ◽  
Neural Tissue ◽  
Apoptotic Cell Death ◽  
Neural Cells ◽  
Cord Injury

Introduction: Necroptosis is a form of programmed cell death that is different from apoptotic cell death. Receptor-interacting protein kinase 1 (RIPK1) plays a particularly important function in necroptosis execution. This study investigated changes in expression of RIPK1 in secondary neural tissue damage following spinal cord injury in mice. The time course of the RIPK1 expression was also compared with that of apoptotic cell death in the lesion site. Methods and Materials: Immunostaining for RIPK1 was performed at different time points after spinal cord injury. The protein expressions of RIPK1 were determined by western blot. The RIPK1 expressions in various neural cells were investigated using immunohistochemistry. To investigate the time course of apoptotic cell death, TUNEL-positive cells were counted at the different time points. To compare the incidence of necroptosis and apoptosis, the RIPK1-labeled sections were co-stained with TUNEL. Results: The RIPK1 expression was significantly upregulated in the injured spinal cord. The upregulation of RIPK1 expression was observed in neurons, astrocytes, and oligodendrocytes. The increase in RIPK1 expression started at 4 hours and peaked at 3 days after injury. Time course of the RIPK1 expression was similar to that of apoptosis detected by TUNEL. Interestingly, the increased expression of RIPK1 was rarely observed in the TUNEL-positive cells. Furthermore, the number of RIPK1-positive cells was significantly higher than that of TUNEL-positive cells. Conclusions: This study demonstrated that the expression of RIPK1 increased in various neural cells and peaked at 3 days following spinal cord injury. The temporal change of the RIPK1 expression was analogous to that of apoptosis at the lesion site. However, the increase in RIPK1 expression was barely seen in the apoptotic cells. These findings suggested that the RIPK1 might contribute to the pathological mechanism of the secondary neural tissue damage after spinal cord injury.

scholarly journals Tetrahydropalmatine reduces cell death and improves functional recovery after traumatic spinal cord injury in ratsTetrahydropalmatine reduces cell death and improves functional recovery after traumatic spinal cord injury in rats

2021 ◽  
Vol 18 (4) ◽  
pp. 703-711
Author(s):  
Haihu Hao ◽  
Qiang Liu ◽  
Dou Wu ◽  
Hao Xing ◽  
Yahui Geng
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Functional Recovery ◽  
Inflammatory Mediators ◽  
Apoptotic Index ◽  
Tunel Assay ◽  
Traumatic Spinal Cord Injury ◽  
Cord Injury

Purpose: To investigate the effectiveness of tetrahydropalmatine (THP) in the treatment of spinal cord injury (SCI) in rats. Methods: Adult Sprague Dawley rats were divided into 3 groups: normal control group, SCI group, and SCI group treated with THP (100 mg kg-1). The effect of THP on spinal cord water content, levels of inflammatory mediators, oxidative stress and apoptosis were determined. Locomotor activity in rats was measured using Basso, Beattie and Bresnahan (BBB) scores. Various oxidative stress markers as well as cytokine levels (NF-ĸB, IL-6, IL-1β and TNF-α were determined. Apoptotic index was measured using TUNEL assay. Results: After 72 h of treatment with THP, BBB scores in SCI group of rats significantly increased from 4.19 ± 0.41 to 8.89 ± 0.47 (p < 0.05). Tunel assay revealed a higher apoptotic index (42.50 ± 3.19) in the tissues of SCI rats than in SCI rats treated with THP (31.48 ± 1.19, p < 0.01). Expressions of inflammatory cytokines were significantly upregulated in SCI rats. However, THP administration resulted in significant downregulation of the expressions (p < 0.01). Conclusion: These results indicate that THP attenuates traumatic SCI in rats via modulation of the levels of anti-inflammatory mediators. Thus, THP has a promising potential for the management of SCI.

Substance P reduces apoptotic cell death possibly by modulating the immune response at the early stage after spinal cord injury

Neuroreport ◽  
2013 ◽  
Vol 24 (15) ◽  
pp. 846-851 ◽  
Author(s):  
Mei Hua Jiang ◽  
Ji Eun Lim ◽  
Guang Fan Chi ◽  
Woosung Ahn ◽  
Mingzi Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Immune Response ◽  
Cell Death ◽  
Substance P ◽  
Apoptotic Cell ◽  
Early Stage ◽  
Apoptotic Cell Death ◽  
Cord Injury
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