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Fang Fang Zhang

Researcher at Hiroshima University

Publications -  21
Citations -  648

Fang Fang Zhang is an academic researcher from Hiroshima University. The author has contributed to research in topics: Neuropathic pain & Nociception. The author has an hindex of 15, co-authored 21 publications receiving 512 citations.

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Neuropathic Pain in Rats with a Partial Sciatic Nerve Ligation Is Alleviated by Intravenous Injection of Monoclonal Antibody to High Mobility Group Box-1

TL;DR: The results demonstrate that nerve injury evokes the synthesis and release of HMGB1 from spinal neurons, facilitating the activity of both microglia and neurons, which in turn leads to symptoms of neuropathic pain, and could be a useful therapeutic strategy in the treatment of chronic pain.
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Amitriptyline up-regulates connexin43-gap junction in rat cultured cortical astrocytes via activation of the p38 and c-Fos/AP-1 signalling pathway.

TL;DR: A potentially novel mechanism of tricyclic antidepressants is to increase the expression and functioning of gap junctions in astrocytes, which is crucial for maintaining CNS homeostasis.
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Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice.

TL;DR: Modulation of Cx43 is suggested as a novel target for developing analgesics for neuropathic pain following peripheral nerve injury and the sensitized state following PSNL is likely maintained by dysfunctional glutamatergic neurotransmission.
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Spinal astrocytes stimulated by tumor necrosis factor‐α and/or interferon‐γ attenuate connexin 43‐gap junction via c‐jun terminal kinase activity

TL;DR: The results indicate that intercellular communication of astrocytes is significantly disrupted in the inflammatory state and that stimulation of spinal astroCytes with inflammatory cytokines leads to significant inhibition of Cx43‐GJIC through activation of the JNK signaling pathway.
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Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy.

TL;DR: It is demonstrated that the maintenance of the neuropathic state following an injured nerve is dependent on the up‐regulation of HMGB1 and MMP‐9, and blockingHMGB1 function in sciatic nerve could be a potent therapeutic strategy for the treatment of neuropathic pain.