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Start Over Author "Kun Chen" Topic inflammation Publisher springer nature
2 results on '"Kun Chen"'

1. Long-term Therapeutic Effects of Extracorporeal Shock Wave-Assisted Melatonin Therapy on Mononeuropathic Pain in Rats.

Author

Yang, Chien-Hui, Yip, Hon-Kan, Chen, Hung-Fei, Yin, Tsung-Cheng, Chiang, John Y., Sung, Pei-Hsun, Lin, Kun-Chen, Tsou, Yu-Huan, Chen, Yi-Ling, Li, Yi-Chen, Huang, Tien-Hung, Huang, Chi-Ruei, Luo, Chi-Wen, and Chen, Kuan-Hung

Subjects
SODIUM channels, DORSAL root ganglia, PAIN management, SCIATIC nerve, SHOCK waves, PROTEIN expression
Abstract

We evaluated the ability of extracorporeal shock wave (ECSW)-assisted melatonin (Mel) therapy to offer an additional benefit for alleviating the neuropathic pain (NP) in rats. Left sciatic nerve was subjected to chronic constriction injury (CCI) to induce NP. Animals (n = 30) were randomized into group 1 (sham-operated control), group 2 (CCI only), group 3 (CCI + ECSW), group 4 (CCI + Mel) and group 5 (CCI + ECSW + Mel). By days 15, 22 and 29 after CCI, the thermal paw withdrawal latency (TPWL) and mechanical paw withdrawal threshold (MPWT) were highest in group 1, lowest in group 2, significantly higher in group 5 than in groups 3 and 4, but they showed no difference between the later two groups (all p < 0.0001). The protein expressions of inflammatory (TNF-α, NF-κB, MMP-9, IL-1ß), oxidative-stress (NOXs-1, -2, -4, oxidized protein), apoptotic (cleaved-caspase3, cleaved-PARP), DNA/mitochondrial-damaged (γ-H2AX/cytosolic-cytochrome C), microglia/astrocyte activation (ox42/GFAP), and MAPKs [phosphorylated (p)-p38, p-JNK, p-ERK] biomarkers in dorsal root ganglia neurons (DRGs) and in spinal dorsal horn were exhibited an opposite pattern of TPWL among the five groups (all p < 0.0001). Additionally, protein expressions of Nav.1.3, Nav.1.8 and Nav.1.9 in sciatic nerve exhibited an identical pattern to inflammation among the five groups (all p < 0.0001). The numbers of cellular expressions of MAPKs (p-ERK1/2+/peripherin + cells, p-ERK1/2+/NF200 + cells and p-JNK+/peripherin + cells, p-JNK+/NF200 + cells) and voltage-gated sodium channels (Nav.1.8+/peripherin + cells, Nav.1.8+/NF200 + cells, Nav.1.9+/peripherin + cells, Nav.1.9+/NF200 + cells) in small and large DRGs displayed an identical pattern to inflammation among the five groups (all p < 0.0001). In conclusion, the synergistic effect of combined ECSW-Mel therapy is superior to either one alone for long-term improvement of mononeuropathic pain-induced by CCI in rats. [ABSTRACT FROM AUTHOR]

Published
2019
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2. Reactive astrocytes undergo M1 microglia/macrohpages-induced necroptosis in spinal cord injury

Author

Hong Fan, Kun Zhang, Fang Kuang, Kun Chen, Gong Ju, Heng Ma, Keqing Zhu, Lequn Shan, and Ya-Zhou Wang

Subjects
0301 basic medicine, Programmed cell death, Pathology, medicine.medical_specialty, Necroptosis, Clinical Neurology, Apoptosis, Spinal cord injury, 03 medical and health sciences, Cellular and Molecular Neuroscience, 0302 clinical medicine, medicine, Animals, Molecular Biology, Spinal Cord Injuries, Inflammation, Mice, Knockout, Neurons, Microglia, biology, business.industry, Macrophages, M1 microglia/macrophage, medicine.disease, Astrogliosis, Cell biology, Toll-Like Receptor 4, Transplantation, Disease Models, Animal, Oligodendroglia, 030104 developmental biology, medicine.anatomical_structure, Spinal Cord, Astrocytes, TLR4, biology.protein, Reactive astrocytes, Neurology (clinical), business, 030217 neurology & neurosurgery, Research Article, Neurotrophin, Astrocyte
Abstract

Background A unique feature of the pathological change after spinal cord injury (SCI) is the progressive enlargement of lesion area, which usually results in cavity formation and is accompanied by reactive astrogliosis and chronic inflammation. Reactive astrocytes line the spinal cavity, walling off the lesion core from the normal spinal tissue, and are thought to play multiple important roles in SCI. The contribution of cell death, particularly the apoptosis of neurons and oligodendrocytes during the process of cavitation has been extensively studied. However, how reactive astrocytes are eliminated following SCI remains largely unclear. Results By immunohistochemistry, in vivo propidium iodide (PI)-labeling and electron microscopic examination, here we reported that in mice, reactive astrocytes died by receptor-interacting protein 3 and mixed lineage kinase domain-like protein (RIP3/MLKL) mediated necroptosis, rather than apoptosis or autophagy. Inhibiting receptor-interacting protein 1 (RIP1) or depleting RIP3 not only significantly attenuated astrocyte death but also rescued the neurotrophic function of astrocytes. The astrocytic expression of necroptotic markers followed the polarization of M1 microglia/macrophages after SCI. Depleting M1 microglia/macrophages or transplantation of M1 macrophages could significantly reduce or increase the necroptosis of astrocytes. Further, the inflammatory responsive genes Toll-like receptor 4 (TLR4) and myeloid differentiation primary response gene 88 (MyD88) are induced in necroptotic astrocytes. In vitro antagonizing MyD88 in astrocytes could significantly alleviate the M1 microglia/macrophages-induced cell death. Finally, our data showed that in human, necroptotic markers and TLR4/MyD88 were co-expressed in astrocytes of injured, but not normal spinal cord. Conclusion Taken together, these results reveal that after SCI, reactive astrocytes undergo M1 microglia/macrophages-induced necroptosis, partially through TLR/MyD88 signaling, and suggest that inhibiting astrocytic necroptosis may be beneficial for preventing secondary SCI. Electronic supplementary material The online version of this article (doi:10.1186/s13024-016-0081-8) contains supplementary material, which is available to authorized users.

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