1.姜黃素抑制星形膠質(zhì)細胞和小膠質(zhì)細胞中脂多糖誘導(dǎo)的趨化因子的表達

2.TLR8 and its endogenous ligand miR-21 contribute to neuropathic pain in murine DRG（TLR8（TOLL樣受體）及其內(nèi)源性配體miR-21對小鼠DRG神經(jīng)性疼痛的作用）

3.慢性疼痛的分子機制和鎮(zhèn)痛新靶點研究

4.細胞色素酶CYP26A1在制備治療神經(jīng)病理性疼痛的藥物中的應(yīng)用

5.靶向神經(jīng)炎癥治療慢性疼痛的療效和機制研究

6.Demethylation of G-Protein-Coupled Receptor 151 Promoter Facilitates the Binding of Kruppel-Like Factor 5 and Enhances Neuropathic Pain after Nerve Injury in Mice（G 蛋白偶聯(lián)受體151啟動子去甲基化促進小鼠神經(jīng)損傷后 kruppel 樣因子5的結(jié)合并增強神經(jīng)性疼痛）

7.Chemokine receptor CCR2 contributes to neuropathic pain and the associated depression via increasing NR2B-mediated currents in both D1 and D2 dopamine receptor-containing medium spiny neurons in the nucleus accumbens shell（趨化因子受體CCR2通過增加伏隔核殼中D1和D2多巴胺受體介導(dǎo)的中棘神經(jīng)元中NR2B介導(dǎo)的電流，促進神經(jīng)性疼痛和相關(guān)抑郁癥）