International immunopharmacology
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Int. Immunopharmacol. · Jan 2020
Hydrogen alleviated organ injury and dysfunction in sepsis: The role of cross-talk between autophagy and endoplasmic reticulum stress: Experimental research.
Sepsis is defined as a life-threatening organ dysfunction that is caused by a dysregulated host response to infection. Although much progress has been made in understanding the pathophysiology of sepsis, further discussion and study of the detailed therapeutic mechanisms are needed. Autophagy and endoplasmic reticulum stress are two pathways of the complicated regulatory network of sepsis. Herein, we focus on the cellular mechanism in which autophagy and endoplasmic reticulum stress participate in hydrogen (H2)-protected sepsis-induced organ injury. ⋯ Hydrogen provided protection from organ injury induced by sepsis via autophagy activation and endoplasmic reticulum stress pathway inactivation.
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Angioedema (AE) occurring during ACE inhibitor therapy (ACEi-AE) is a rare complication involving between 0.1 and 0.7% of treated patients. AE can also complicate other therapeutic regimens that block the renin-angiotensin aldosterone system. Other drugs, such as immune suppressors, some type of antidiabetics or calcium antagonists, can increase the likelihood of ACEi-AE when associated to ACEi. ⋯ Corticosteroids and antihistamines do not show efficacy. Some therapeutic attempts have shown some efficacy for fresh frozen plasma or C1 inhibitor concentrate infusion. Interventional studies with the specific bradykinin receptor antagonist icatibant have shown conflicting results; there might be a different ethnic predisposition to icatibant efficacy which has been proven in caucasian but not in black patients.
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Int. Immunopharmacol. · Jan 2020
Human bone mesenchymal stem cells-derived exosomes overexpressing microRNA-26a-5p alleviate osteoarthritis via down-regulation of PTGS2.
Osteoarthritis (OA) is a degenerative disease characterized by synovium inflammation and articular cartilage damage. The aberrant expression profile of microRNAs (miRNAs) has been implicated in the cartilage of patients with OA. However, how microRNAs carried by exosomes derived from mesenchymal stem cells (MSCs) associated with OA progression is still unknown. ⋯ Additionally, the overexpression of miR-26a-5p exerted an alleviatory effect on the damage of the synovial fibroblasts by repressing PTGS2. Moreover, hBMSC-derived exosomes overexpressing miR-26a-5p retarded damage of synovial fibroblasts in vitro and alleviated OA damage in vivo. Taken together, hBMSC-derived exosomes overexpressing miR-26a-5p serve as a repressor for damage of synovial fibroblasts via PTGS2 in OA, which is of significance for the treatment of OA in rats.