And interpreted the pathological data. CJC performed mouse genotyping, analyzed theAnd interpreted the pathological data.

And interpreted the pathological data. CJC performed mouse genotyping, analyzed the
And interpreted the pathological data. CJC performed mouse genotyping, analyzed the pathological behavioral data, and performed immunocytochemistry. YWL performed the electrophysiology. CCC oversaw PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27107493 the research and prepared the manuscript with help from all others.Additional material Additional fileInflammation-mediated hyperalgesia in the contralateral paws. A, Thermal hyperalgesia results of intraplantar inflammation. B, von Frey filament test results of intraplantar inflammation. C, Thermal hyperalgesia results of intramuscular inflammation. D, von Frey filament tests results of intramuscular inflammation. WT: ASIC3+/+ mice, n = 6 in each group. KO: ASIC3-/- mice, n = 6 in each group. *p < 0.05 compared to baseline latency. #p < 0.05 comparison between ASIC3+/+ and ASIC3-/groups. Click here for file [http://www.biomedcentral.com/content/supplementary/17448069-5-1-S1.pdf]Page 14 of(page number not for citation purposes)Molecular Pain 2009, 5:http://www.molecularpain.com/content/5/1/Additional fileGene expression level in ASIC3+/+ DRG 2 days after induction of inflammation. A, Expression of ASIC3, Nav1.6, Nav1.7, Nav1.8, Nav1.9 and TRPV1 2 days after intraplantar carrageenan-induced inflammation in L5 DRG. B, Expression of ASIC3, Nav1.6, Nav1.7, Nav1.8, Nav1.9 and TRPV1 2 days after intramuscular inflammation induction in L4 DRG. *p < 0.05 compared with saline group of the same side. Click here for file [http://www.biomedcentral.com/content/supplementary/17448069-5-1-S2.pdf]17. 18. 19. 20.21.AcknowledgementsThe work was supported by PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28914615 National Science Council grants NSC 93-2320B-001-047, NSC 94-2320-B-001-039 and NSC 96-2311-B-001-041-MY2. We thank Dr. Takeki Kikuchi for help in pathological examination and Mr. Shing-Hong Lin for help in statistics. 22. 23. 24.
Lan et al. Molecular Pain 2010, 6:2 http://www.molecularpain.com/content/6/1/MOLECULAR PAINOpen AccessRESEARCHDown-regulation of Toll-like receptor 4 gene expression by short interfering RNA attenuates bone cancer pain in a rat modelLiu Si Lan1,2*, Yang Jian Ping1*, Wang Li Na1, Jiang Miao1, Qiu Qiao Cheng1, Ma Zhen Ni1, Liu Lei1, Li Cai Fang1, Ren Chun Guang1, Zhou Jin1, Li WeiAbstractBackground: This study demonstrates a critical role in CNS innate immunity of the microglial Toll-like receptor 4 (TLR4) in the induction and maintenance of behavioral hypersensitivity in a rat model of bone cancer pain with the technique of RNA interference (RNAi). We hypothesized that after intramedullary injection of Walker 256 cells (a breast cancer cell line) into the tibia, CNS neuroimmune activation and subsequent cytokine expression are triggered by the stimulation of microglial membrane-bound TLR4. Results: We assessed tactile allodynia and spontaneous pain in female Sprague-Dawley (SD) rats after intramedullary injection of Walker 256 cells into the tibia. In a complementary study, TLR4 small interfering RNA (siRNA) was administered intrathecally to bone cancer pain rats to reduce the expression of spinal TLR4. The bone cancer pain rats treated with TLR4 siRNA displayed significantly attenuated behavioral hypersensitivity and decreased expression of spinal microglial markers and proinflammatory cytokines compared with controls. Only intrathecal injection of TRL4 siRNA at post-inoculation day 4 could prevent initial Oxaliplatin biological activity development of bone cancer pain; intrathecal injection of TRL4 siRNA at post-inoculation day 9 could attenuate, but not completely block, wellestablished bone cancer pain. Con.