β-Elemene Enhances GAP-43 Expression and Neurite Outgrowth by Inhibiting RhoA Kinase Activation in Rats with Spinal Cord Injury

Wang, Jingyu; Li, Heyangzi; Yao, Ying; Ren, Yucheng; Lin, Jiangtao; Hu, Jue; Zheng, Mingfeng; Song, Xinghui; Zhao, Tengfei; Chen, Yingying; Shen, Yue‐Liang; Zhu, Yongjian; Wang, Lin-Lin

doi:10.1016/j.neuroscience.2018.04.045

Cited by 24 publications

(13 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For CCK-8 (#C0041, Beyotime Institute of Biotechnologu, Nangtong, Jiangsu, China) assay, VSC4.1 motor neurons (1 × 10 4 cells/well) were seeded into 96-well plates after digestion with trypsin and five parallel wells were used for each treatment. The survival of post-OGD VSC4.1 motor neurons was assayed using a CCK-8 Kit (#C0037, Beyotime Institute of Biotechnology, Nantong, Jiangsu, China) as previously described 34. After incubating for 2 h, cell viability was calculated by TECAN infinite M5 (Molecular Devices, USA) at the wavelength of 450 nm.…”

Section: Methodsmentioning

confidence: 99%

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

et al. 2019

Self Cite

View full text Add to dashboard Cite

Recent studies have demonstrated that bone marrow mesenchymal stem cells (BMSCs) protect the injured neurons of spinal cord injury (SCI) from apoptosis while the underlying mechanism of the protective effect of BMSCs remains unclear. In this study, we found the transfer of mitochondria from BMSCs to injured motor neurons and detected the functional improvement after transplanting. Methods: Primary rat BMSCs were co-cultured with oxygen-glucose deprivation (OGD) injured VSC4.1 motor neurons or primary cortical neurons. FACS analysis was used to detect the transfer of mitochondria from BMSCs to neurons. The bioenergetics profiling of neurons was detected by Extracellular Flux Analysis. Cell viability and apoptosis were also measured. BMSCs and isolated mitochondria were transplanted into SCI rats. TdT-mediated dUTP nick end labelling staining was used to detect apoptotic neurons in the ventral horn. Immunohistochemistry and Western blotting were used to measure protein expression. Re-myelination was examined by transmission electron microscope. BBB scores were used to assess locomotor function. Results: MitoTracker-Red labelled mitochondria of BMSCs could be transferred to the OGD injured neurons. The gap junction intercellular communication (GJIC) potentiator retinoid acid increased the quantity of mitochondria transfer from BMSCs to neurons, while GJIC inhibitor 18β glycyrrhetinic acid decreased mitochondria transfer. Internalization of mitochondria improved the bioenergetics profile, decreased apoptosis and promoted cell survival in post-OGD motor neurons. Furthermore, both transplantation of mitochondria and BMSCs to the injured spinal cord improved locomotor functional recovery in SCI rats. Conclusions: To our knowledge, this is the first evidence that BMSCs protect against SCI through GJIC to transfer mitochondrial to the injured neurons. Our findings suggested a new therapy strategy of mitochondria transfer for the patients with SCI.

show abstract

Section: Methodsmentioning

confidence: 99%

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

et al. 2019

Self Cite

View full text Add to dashboard Cite

show abstract

“…it has also been found that Y-27632 promotes neurite outgrowth in Pc12 cells (9). Y-27632 has also been used in treatments following spinal cord injury, for it is known to promote neurite outgrowth and axonal regeneration in neurons (10). However, the effect of Y-27632 on cir injury needs to be studied.…”

Section: Introductionmentioning

confidence: 99%

ROCK inhibitor Y‑27632 protects rats against cerebral ischemia/reperfusion‑induced behavioral deficits and hippocampal damage

Li¹,

Liu²

2019

Mol Med Report

View full text Add to dashboard Cite

cerebral ischemic injury is a major cause of death and long-term disability worldwide that leads to neurological and behavioral deficits, and for which successful treatments are still lacking. ras homolog family member a (rhoa) and rho-associated coiled-coil containing protein kinase (rocK) are associated with the growth of neurons and the movement of neuronal growth cones. rhoa/rocK inhibitors have been demonstrated to promote the recovery of motor function following nerve injury, but the underlying mechanism requires further investigation. The present study aimed to investigate the effects of the rocK inhibitor Y-27632 on middle cerebral artery occlusion (Mcao)-induced cerebral ischemic injury. rats were randomly assigned to the control, Y-27632, Mcao + Vehicle or Mcao + Y-27632 group. Firstly, infarct volume, cognitive ability and cerebral injury were assessed. Secondly, indicators of cerebral inflammation, oxidative stress and apoptosis were evaluated. Finally, the expression of recombinant glial fibrillary acidic protein (GFaP) and allograft inflammatory factor 1 (aiF1) in the brain were measured to assess the activation of astrocytes and microglia, respectively. The results showed that Y-27632 effectively increased the survival rate and behavioral performance of rats, and attenuated the cerebral injury, oxidative stress and cerebral inflammation levels following MCAO. The disturbance in hippocampal neurons caused by Mcao was also alleviated following treatment with Y-27632. neuronal apoptosis was also decreased following Y-27632 treatment, as demonstrated by the Tunel assay and the expression levels of caspases-3, 8 and 9 and Bax/Bcl-2 ratio. The levels of GFaP and aiF1 were increased by Mcao and further promoted by Y-27632, indicating the activation of astrocytes and microglia. in conclusion, the present study offered evidence of a protective effect of Y-27632 administration on cerebral ischemia/reperfusion induced behavioral and hippocampal damage by activating astrocytes and microglia.

show abstract

“…After 24 hours, the viability of the ADSCs and cytotoxic effects were determined using a CCK-8 kit (Dojindo, Japan) and a LDH release kit (Beyotime Institute of Biotechnology, Jiangsu, China), respectively, according to the manufacturer’s instructions. 15 , 16 …”

Section: Methodsmentioning

confidence: 99%

Co-transfection with BMP2 and FGF2 via chitosan nanoparticles potentiates osteogenesis in human adipose-derived stromal cells in vitro

Zhao

Fang

et al. 2021

J Int Med Res

View full text Add to dashboard Cite

Objective To investigate if co-transfection of human bone morphogenetic protein 2 (BMP-2, BMP2) and human fibroblast growth factor 2 (FGF2, FGF2) via chitosan nanoparticles promotes osteogenesis in human adipose tissue-derived stem cells (ADSCs) in vitro. Materials and Methods Recombinant BMP2 and/or FGF2 expression vectors were constructed and packaged into chitosan nanoparticles. The chitosan nanoparticles were characterized by atomic force microscopy. Gene and protein expression levels of BMP-2 and FGF2 in ADSCs in vitro were evaluated by real-time polymerase chain reaction (PCR), western blot, and enzyme-linked immunosorbent assay. Osteocalcin (OCN) and bone sialoprotein (BSP) gene expression were also evaluated by real-time PCR to assess osteogenesis. Results The prepared chitosan nanoparticles were spherical with a relatively homogenous size distribution. The BMP2 and FGF2 vectors were successfully transfected into ADSCs. BMP-2 and FGF2 mRNA and protein levels were significantly up-regulated in the co-transfection group compared with the control group. OCN and BSP mRNA levels were also significantly increased in the co-transfection group compared with cells transfected with BMP2 or FGF2 alone, suggesting that co-transfection significantly enhanced osteogenesis. Conclusions Co-transfection of human ADSCs with BMP2/FGF2 via chitosan nanoparticles efficiently promotes the osteogenic properties of ADSCs in vitro.

show abstract

β-Elemene Enhances GAP-43 Expression and Neurite Outgrowth by Inhibiting RhoA Kinase Activation in Rats with Spinal Cord Injury

Cited by 24 publications

References 31 publications

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

ROCK inhibitor Y‑27632 protects rats against cerebral ischemia/reperfusion‑induced behavioral deficits and hippocampal damage

Co-transfection with BMP2 and FGF2 via chitosan nanoparticles potentiates osteogenesis in human adipose-derived stromal cells in vitro

Contact Info

Product

Resources

About