Objective: To investigate the effect of flurbiprofen axetil analgesia after knee replacement on the cytokine contents in serum and joint fluid as well as HPA axis activity. Methods: Patients who underwent knee replace...Objective: To investigate the effect of flurbiprofen axetil analgesia after knee replacement on the cytokine contents in serum and joint fluid as well as HPA axis activity. Methods: Patients who underwent knee replacement in People's Hospital of Dongxihu District between April 2015 and January 2018 were selected as the research subjects and randomly divided into the experimental group who accepted flurbiprofen axetil combined with patient-controlled intravenous analgesia and the control group who accepted patient-controlled intravenous analgesia alone. The contents of cytokines and HPA axis-related hormones in serum were measured before surgery as well as 1 d and 3 d after surgery;the contents of cytokines in joint fluid were measured 1 d and 3 d after surgery. Results: Compared with those of same group before surgery, NGF, NPY, TNF-α, IL-2, IL-4, IL-10, ACTH, COR, INS, GH and PRL levels of both groups were increasing 1 d and 3 d after surgery, and NGF, NPY, TNF-α, IL-2, IL-4, IL-10, ACTH, COR, INS, GH and PRL levels in serum as well as PGE2, OPN, TGF-β1, FGF21, CXCL12 and YKL-40 in joint fluid of experimental group 1 d and 3 d after surgery were lower than those of control group. Conclusion: Flurbiprofen axetil analgesia after knee replacement can reduce the release of cytokines in serum and joint fluid, and inhibit the activity of HPA axis, and its analgesic effect is exact.展开更多
The present study was designed to investigate the possible role ofHPA （hypothalamic-pituitary-adrenal） axis in neuropathic pain in streptozotocin induced diabetic rats. Wistar albino rats of either sex weighing 180-...The present study was designed to investigate the possible role ofHPA （hypothalamic-pituitary-adrenal） axis in neuropathic pain in streptozotocin induced diabetic rats. Wistar albino rats of either sex weighing 180-220 g （n = 6） were employed. Diabetes was induced by administering STZ （streptozotocin） （45 mg/kg, i.p.） once. Neuropathy was induced by the ligation of sciatic nerve in diabetic animals. A glucocorticoid receptor antagonist： ketoconazole 175 mg/kg, p.o. and glucocorticoid receptor agonist： hydrocortisone 1 mg/kg, i.p. were given. Assessment of neuropathic pain was achieved using hot plate and hot immersion tests. Tissue biochemical： lipid peroxidation, NO and glutathione were estimated on 28th day spectrophotometrically. Plasma cortisol level was also estimated using HPLC （high performance liquid chromatography）. Sciatic nerve ligation to diabetic animals caused significant increase in nociceptive responses as hyperalgesia and allodynia, tissue lipid peroxidation and NO products, and decrease in GSH （glutathione） level, in comparison to SC （saline control）. Ketoconazole administration produced decreased pain responses as well as decrease in oxidative stress and inflammatory mediators. Administration of hydrocortisone resulted in suppression of HPA axis. The activation of HPA axis in diabetic animals resulted in significant pain response. This may be due to increased corticosterone level which in turn desensitizes HPA axis and decreased nociceptive response in diabetic animals observed.展开更多
Accumulating studies have proved that perinatal exposure to environmental dose causes long-term potentiation in anxiety/depression-related behaviors in rats. Hyperactivity of the hypothalamic-pituitary-adrenal （HPA）...Accumulating studies have proved that perinatal exposure to environmental dose causes long-term potentiation in anxiety/depression-related behaviors in rats. Hyperactivity of the hypothalamic-pituitary-adrenal （HPA） axis is one of the most consistent biological findings in anxiety- and depression-related disorders. The HPA axis is reported to be susceptible to developmental reprogramming. The present study focused on HPA reactivity in postnatal day （PND） 80 male rats exposed perinatally to environmental-dose BPA. When female breeders were orally administered 2 μg/（kg.day） BPA from gestation day 10 to lactation day 7, their offspring （PND 80 BPA-exposed rats） showed obvious anxiety/depression-like behaviors. Notably, significant increase in serum corticosterone and adrenocorticotropin, and corticotropin-releasing hormone mRNA were detected in BPA-exposed rats before or after the mild stressor. Additionally, the level of glucocorticoid receptor mRNA in the hippocampus, but not the hypothalamus, was decreased in BPA-exposed rats. The levels of hippocampal mineralocorticoid receptor mRNA, neuronal nitric oxide synthase and phosphorylated cAMP response element binding protein were increased in BPA-exposed rats. In addition, the testosterone level was in BPA-exposed rats. The results indicate that reprogramming-induced hyperactivity of the HPA axis is an important link between perinatal BPA exposure and persistent potentiation in anxiety and depression.展开更多
Anxiety disorder is a common and serious mental disorder.At present,the pathogenesis of anxiety disorder includes hypothalamus-pituitary-adrenal(HPA)axis,neuroimmune,and brain-gut axis disorders,among others.This pape...Anxiety disorder is a common and serious mental disorder.At present,the pathogenesis of anxiety disorder includes hypothalamus-pituitary-adrenal(HPA)axis,neuroimmune,and brain-gut axis disorders,among others.This paper discusses the correlation between anx-iety disorder and the hypothalamus-pituitary-endocrine axis and finds that immune inflammation can be used as a“bridge”between the hypothalamus-pituitary-endocrine axis and anxiety disorder.展开更多
文摘Objective: To investigate the effect of flurbiprofen axetil analgesia after knee replacement on the cytokine contents in serum and joint fluid as well as HPA axis activity. Methods: Patients who underwent knee replacement in People's Hospital of Dongxihu District between April 2015 and January 2018 were selected as the research subjects and randomly divided into the experimental group who accepted flurbiprofen axetil combined with patient-controlled intravenous analgesia and the control group who accepted patient-controlled intravenous analgesia alone. The contents of cytokines and HPA axis-related hormones in serum were measured before surgery as well as 1 d and 3 d after surgery;the contents of cytokines in joint fluid were measured 1 d and 3 d after surgery. Results: Compared with those of same group before surgery, NGF, NPY, TNF-α, IL-2, IL-4, IL-10, ACTH, COR, INS, GH and PRL levels of both groups were increasing 1 d and 3 d after surgery, and NGF, NPY, TNF-α, IL-2, IL-4, IL-10, ACTH, COR, INS, GH and PRL levels in serum as well as PGE2, OPN, TGF-β1, FGF21, CXCL12 and YKL-40 in joint fluid of experimental group 1 d and 3 d after surgery were lower than those of control group. Conclusion: Flurbiprofen axetil analgesia after knee replacement can reduce the release of cytokines in serum and joint fluid, and inhibit the activity of HPA axis, and its analgesic effect is exact.
文摘The present study was designed to investigate the possible role ofHPA （hypothalamic-pituitary-adrenal） axis in neuropathic pain in streptozotocin induced diabetic rats. Wistar albino rats of either sex weighing 180-220 g （n = 6） were employed. Diabetes was induced by administering STZ （streptozotocin） （45 mg/kg, i.p.） once. Neuropathy was induced by the ligation of sciatic nerve in diabetic animals. A glucocorticoid receptor antagonist： ketoconazole 175 mg/kg, p.o. and glucocorticoid receptor agonist： hydrocortisone 1 mg/kg, i.p. were given. Assessment of neuropathic pain was achieved using hot plate and hot immersion tests. Tissue biochemical： lipid peroxidation, NO and glutathione were estimated on 28th day spectrophotometrically. Plasma cortisol level was also estimated using HPLC （high performance liquid chromatography）. Sciatic nerve ligation to diabetic animals caused significant increase in nociceptive responses as hyperalgesia and allodynia, tissue lipid peroxidation and NO products, and decrease in GSH （glutathione） level, in comparison to SC （saline control）. Ketoconazole administration produced decreased pain responses as well as decrease in oxidative stress and inflammatory mediators. Administration of hydrocortisone resulted in suppression of HPA axis. The activation of HPA axis in diabetic animals resulted in significant pain response. This may be due to increased corticosterone level which in turn desensitizes HPA axis and decreased nociceptive response in diabetic animals observed.
基金supported by China Postdoctoral Science Foundation(2013M540456)Jiangsu Planned Projects for Postdoctoral Research Funds(1301065B)+3 种基金Grants for 973(2014CB943303)NSFC(810710273117144081000482)
文摘Accumulating studies have proved that perinatal exposure to environmental dose causes long-term potentiation in anxiety/depression-related behaviors in rats. Hyperactivity of the hypothalamic-pituitary-adrenal （HPA） axis is one of the most consistent biological findings in anxiety- and depression-related disorders. The HPA axis is reported to be susceptible to developmental reprogramming. The present study focused on HPA reactivity in postnatal day （PND） 80 male rats exposed perinatally to environmental-dose BPA. When female breeders were orally administered 2 μg/（kg.day） BPA from gestation day 10 to lactation day 7, their offspring （PND 80 BPA-exposed rats） showed obvious anxiety/depression-like behaviors. Notably, significant increase in serum corticosterone and adrenocorticotropin, and corticotropin-releasing hormone mRNA were detected in BPA-exposed rats before or after the mild stressor. Additionally, the level of glucocorticoid receptor mRNA in the hippocampus, but not the hypothalamus, was decreased in BPA-exposed rats. The levels of hippocampal mineralocorticoid receptor mRNA, neuronal nitric oxide synthase and phosphorylated cAMP response element binding protein were increased in BPA-exposed rats. In addition, the testosterone level was in BPA-exposed rats. The results indicate that reprogramming-induced hyperactivity of the HPA axis is an important link between perinatal BPA exposure and persistent potentiation in anxiety and depression.
文摘Anxiety disorder is a common and serious mental disorder.At present,the pathogenesis of anxiety disorder includes hypothalamus-pituitary-adrenal(HPA)axis,neuroimmune,and brain-gut axis disorders,among others.This paper discusses the correlation between anx-iety disorder and the hypothalamus-pituitary-endocrine axis and finds that immune inflammation can be used as a“bridge”between the hypothalamus-pituitary-endocrine axis and anxiety disorder.
