- 作者: Ling-Yuan Kong; Gwang-Ho Jeohn; Pearlie M. Hudson; Lina Du; Bin Liu; Jau-Shyong Hong
- 作者服務機構: Neuropharmacology Section, Laboratory of Pharmacology and CChemistry, National Institute of Enviornmental Health Sciences, Research Triangle Park, N.C., USA
- 中文摘要: --
- 英文摘要: Previously we reported that ultralow concentrations ofdynorphins (10 to 10 M) inhibited lipopolysaccha-ride (LPS)-induced production of nitric oxide (NO) andproinflammatory cytokines in mouse glia without theparticipation of κ-opioid receptors. In the current studyusing mouse cortical neuron-glia cocultures, we exam-ined the possibility that inhibition of glia inflammatoryresponse by dynorphins might be neuroprotective forneurons. LPS, in a concentration-dependent manner,markedly increased the release of lactate dehydroge-nase (LDH), an indicator of cellular injury. Ultralow con-centrations (10 to 10 M) of dynorphin (dyn) A-(1-8)significantly prevented the LPS-induced release of LDH,loss of neurons, and changes in cell morphology, in addi-tion to inhibition of LPS-induced nitrite production.Meanwhile, ultralow concentrations(10 to 10 M) ofdes-[Tyr ]-dyn A-(2-17), a nonopioid peptide which doesnot bind to κ-opioid receptors, exhibited the same inhibi-tory effect as dyn A-(1-17). These results suggest thatdynorphins at ultralow concentrations are capable ofreducing LPS-induced neuronal injury and these neuro-protective effects of dynorphins are not mediated byclassical opioid receptors.
- 中文關鍵字: --
- 英文關鍵字: --