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Na Li

Researcher at Second Military Medical University

Publications -  17
Citations -  340

Na Li is an academic researcher from Second Military Medical University. The author has contributed to research in topics: Trigeminal ganglion & Receptor. The author has an hindex of 8, co-authored 15 publications receiving 254 citations.

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Methane limit LPS-induced NF-κB/MAPKs signal in macrophages and suppress immune response in mice by enhancing PI3K/AKT/GSK-3β-mediated IL-10 expression

TL;DR: It is shown that methane-rich saline (MS) ip treatment alleviated endotoxin shock, bacteria-induced sepsis and dextran-sulfate-sodium-induced colitis in mice via decreased production of TNF-α and IL-6 and resulted in markedly enhanced phosphorylation of GSK-3β and AKT, which both mediate the release of Il-10.
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Inhibition of G protein-coupled P2Y2 receptor induced analgesia in a rat model of trigeminal neuropathic pain.

TL;DR: It is suggested that inhibition of P2Y2 receptors leads to down-regulation of ERK-mediated phosphorylation and increase of the expression of IA–related Kv channels in trigeminal ganglion neurons, which might contribute to the clinical treatment of trigemINAL neuropathic pain.
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The role of large-conductance, calcium-activated potassium channels in a rat model of trigeminal neuropathic pain

TL;DR: The results indicate the important involvement of mainly ERK and p38 MAPK pathways in modulating BKCa channels in ION-CCI TG neurons, and represent a new therapeutic target for the clinical treatment of trigeminal neuropathic pain.
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Metabolomics coupled with pathway analysis characterizes metabolic changes in response to BDE-3 induced reproductive toxicity in mice.

TL;DR: UHPLC-Q-TOFMS-based metabolomics approach provided a better understanding of PBDEs-induced toxicity dynamically and revealed several pathways including Tyrosine metabolism, Purine metabolism and Riboflavin metabolism, which may give a possible explanation for the toxic mechanism of BDE-3.
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Methane alleviates carbon tetrachloride induced liver injury in mice: anti-inflammatory action demonstrated by increased PI3K/Akt/GSK-3β-mediated IL-10 expression

TL;DR: The data provide evidence that MS may activate the PI3K–AKT–GSK-3β pathway to induce IL-10 expression and produce anti-inflammatory effects via the NF-κB and MAPK pathways and provide a new pharmacological strategy for management of inflammatory response after acute liver injury.