The elevation of body temperature during fever reaction and endogenous antipyretic effect reflects the existing balance between 2 components directed to the maximal positive use of the fever effects and simultaneous prevention of their side effects. The mechanisms involved in the control of balance between factors known as the fever triggers and endogenous antipyretic factors. The possible mechanisms of action of various endogenous antipyretic system components (glucocorticoids, neuropeptides, cytokines etc.) capable to regulate the duration and quantity of fever reaction are discussed in this review.
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Biochem Pharmacol
December 2024
Changning Maternity and Infant Health Hospital and School of Life Sciences, Shanghai Key Laboratory of Regulatory Biology, East China Normal University, Shanghai, PR China. Electronic address:
Preeclampsia is a unique multisystem progressive disease during pregnancy, which seriously endangers the health of pregnant women and fetuses. In clinical practice, aspirin is recommended for the prevention of preeclampsia, but the mechanism by which aspirin prevents preeclampsia has not yet been revealed. This report comprehensively evaluates the effects of aspirin on the expression and activity of placental metabolic enzymes and transporters.
View Article and Find Full Text PDFJ Colloid Interface Sci
January 2025
Department of Pharmacy, Xiangya Hospital, Central South University, Changsha 410008, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, China. Electronic address:
With the rapid advancements in biomedicine, the use of clinical drugs has surged sharply. However, potential hepatotoxicity limits drug exploitation and widespread usage, posing serious threats to patient health. Hepatotoxic drugs disrupt liver enzyme levels and cause refractory pathological damage, creating a challenge in the application of diverse first-line drugs.
View Article and Find Full Text PDFProstaglandins Leukot Essent Fatty Acids
March 2024
Department of Pharmacy, Faculty of Pharmacy, Kindai University, Osaka 577-8502, Japan.
Hepatic microvascular disruption caused by injury to liver sinusoidal endothelial cells (LSECs) is an aggravating factor for drug-induced liver injury (DILI). It is suggested that prostaglandin E (PGE) may be able to attenuate LSEC injury. However, it is also known that 15-keto PGE, a metabolite of PGE produced by 15-prostaglandin dehydrogenase (15-PGDH) that is not a ligand of PGE receptors, suppresses inflammatory acute liver injury as a ligand of peroxisome proliferator-activated receptor γ.
View Article and Find Full Text PDFMetabolites
July 2024
Guangxi Key Laboratory of Zhuang and Yao Ethnic Medicine, The Collaborative Innovation Center of Zhuang and Yao Ethnic Medicine, Guangxi Engineering Research Center of Ethnic Medicine Resources and Application, Guangxi University of Chinese Medicine, Nanning 530200, China.
Biosens Bioelectron
October 2024
Department of Laboratory Medicine and Sichuan Provincial Key Laboratory for Human Disease Gene Study, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610041, China. Electronic address:
Drug-induced liver injury (DILI) poses a severe threat to public health. Endoplasmic reticulum (ER) stress contributes significantly to DILI pathogenesis, with peroxynitrite (ONOO) identified as a pivotal indicator. However, the temporal and spatial fluctuations of ONOO associated with ER stress in the pathogenesis of DILI remain unclear.
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