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Item Current Perspectives of Neuroendocrine Regulation in Liver Fibrosis(MDPI, 2022-11-26) Li, Bowen; Wang, Hui; Zhang, Yudian; Liu, Ying; Zhou, Tiejun; Zhou, Bingru; Zhang, Ying; Chen, Rong; Xing, Juan; He, Longfei; Salinas, Jennifer Mata; Koyama, Sachiko; Meng, Fanyin; Wan, Ying; Medicine, School of MedicineLiver fibrosis is a complicated process that involves different cell types and pathological factors. The excessive accumulation of extracellular matrix (ECM) and the formation of fibrotic scar disrupt the tissue homeostasis of the liver, eventually leading to cirrhosis and even liver failure. Myofibroblasts derived from hepatic stellate cells (HSCs) contribute to the development of liver fibrosis by producing ECM in the area of injuries. It has been reported that the secretion of the neuroendocrine hormone in chronic liver injury is different from a healthy liver. Activated HSCs and cholangiocytes express specific receptors in response to these neuropeptides released from the neuroendocrine system and other neuroendocrine cells. Neuroendocrine hormones and their receptors form a complicated network that regulates hepatic inflammation, which controls the progression of liver fibrosis. This review summarizes neuroendocrine regulation in liver fibrosis from three aspects. The first part describes the mechanisms of liver fibrosis. The second part presents the neuroendocrine sources and neuroendocrine compartments in the liver. The third section discusses the effects of various neuroendocrine factors, such as substance P (SP), melatonin, as well as α-calcitonin gene-related peptide (α-CGRP), on liver fibrosis and the potential therapeutic interventions for liver fibrosis.Item Interpreting Neuroendocrine Hormones, Corticosterone, and Blood Glucose to Assess the Wellbeing of Anesthetized Rats during Euthanasia(American Association for Laboratory Animal Science, 2018-10-10) Hickman, Debra L.; Laboratory Animal Resource Center, IU School of MedicineCurrent recommendations for assessing animal wellbeing during euthanasia suggest that measuring neuroendocrine hormones-such as ACTH, noradrenaline, and adrenaline-is preferable to measuring corticosterone and blood glucose because of the sensitivity of neuroendocrine hormones to the acute stress associated with rapid methods of euthanasia. However, theseneuroendocrine hormones can be stimulated in ways that confound interpretation of welfare assessment in euthanasia studies.Although this property does not negate the usefulness of neuroendocrine hormones as tools of assessment, it is importantto differentiate the stress associated with the induction of anesthesia before the loss of consciousness (an animal wellbeingconcern) with the physiologic responses that occur after the loss of consciousness (not an animal wellbeing concern). In thisstudy, rats were anesthetized by using a ketamine-xylazine combination. Once the rats achieved a surgical plane of anesthesia,they were exposed to O2, CO2, or isoflurane, followed by terminal blood collection to assess concentrations of ACTH,noradrenaline, corticosterone, and blood glucose. Compared with animals exposed to O2 or isoflurane, rats exposed to CO2had significant increases in their serum concentrations of ACTH and noradrenaline, but blood glucose and corticosteronedid not differ between groups. These findings indicate that noradrenaline and ACTH should be used with caution to assessanimal wellbeing when the method of euthanasia might confound that assessment.