title: Interleukin-1β (IL-1β) increases pain behavior and the blood glucose level: possible involvement of glucocorticoid system.
abstract: The possible involvement of glucocorticoid system in interleukin-1β (IL-1β)-induced nociception and the blood glucose level was studied in ICR mice. In the first experiment, mice were treated intrathecally (i.t.) with IL-1β (100 pg). Corticotrophin releasing hormone (CRH) mRNA (hypothalamus) and c-Fos mRNA (pituitary gland, spinal cord, and the adrenal gland) levels were measured at 30, 60 and 120 min after IL-1β administration. We found that i.t. injection with IL-1β increased CRH mRNA level in the hypothalamus. The IL-1β administered i.t. elevated c-Fos mRNA levels in the spinal cord, pituitary and adrenal glands. Furthermore, i.t. administration of IL-1β significantly increased the plasma corticosterone level up to 60 min. In addition, the adrenalectomy caused the reductions of the blood glucose level and pain behavior induced by IL-1β injected i.t. in normal and D-glucose-fed groups. Furthermore, intraperitoneal (i.p.) pretreatment with RU486 (100mg/kg) attenuated the blood glucose level and pain behavior induced by IL-1β administered i.t. in normal and D-glucose-fed groups. Our results suggest that IL-1β administered i.t. increases the blood glucose level and pain behavior via an activation of the glucocorticoid system.
authors.affiliation: Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University, 39 Hallymdaehak-gil, Chuncheon, Gangwon-do 200-702, Republic of Korea.
authors.forename: Yun-Beom
authors.initials: YB
authors.lastname: Sim
authors.forename: Soo-Hyun
authors.initials: SH
authors.lastname: Park
authors.forename: Yu-Jung
authors.initials: YJ
authors.lastname: Kang
authors.forename: Jun-Sub
authors.initials: JS
authors.lastname: Jung
authors.forename: Ohk-Hyun
authors.initials: OH
authors.lastname: Ryu
authors.forename: Moon-Gi
authors.initials: MG
authors.lastname: Choi
authors.forename: Seong-Soo
authors.initials: SS
authors.lastname: Choi
authors.forename: Hong-Won
authors.initials: HW
authors.lastname: Suh
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000315:Adrenalectomy; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects*; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage; D006727:Hormone Antagonists / Q000494:pharmacology; D053583:Interleukin-1beta / Q000378:metabolism*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D015735:Mifepristone / Q000494:pharmacology; D059225:Nociception / Q000187:drug effects*; D010146:Pain / Q000188:drug therapy* / Q000378:metabolism; D010902:Pituitary Gland / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013116:Spinal Cord / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D006727:Hormone Antagonists; D053583:Interleukin-1beta; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D003346:Corticotropin-Releasing Hormone; D005947:Glucose; D003345:Corticosterone
keywords: Adrenalectomy; Blood glucose; CRH; Glucocorticoid; IL-1β; IP; IT; Interleukin-1β; Signal molecules pathway; corticotrophin releasing hormone; interleukin-1β; intraperitoneal; intrathecal