Chronic loss of cardiomyocyte integrity underlies human heart failure associated with aging that often involves progression of acute myocardial infarction and the maladaptive response of cardiomyopathy. SW033291, an inhibitor of 15-prostaglandin dehydrogenase (15-PGDH), has been shown to mitigate fibrosis of mice heart. Whether it has cardioprotective effect remain unknown. Young and aged C57BL/6 J mice were treated with either the vehicle or SW033291 for four weeks. The expression of the target gene was assessed by RT-qPCR, Western blotting, and ELISA. Cardiac function was measured by echocardiography. Our study demonstrated that SW033291 induced a notable upregulation of prostaglandin E2 while concurrently downregulated the expression of both 15-PGDH and troponin I in cardiac tissues, encompassing both young and aged mice. Notably, the administration of SW033291 resulted in a significant improvement in systolic and diastolic function among aged mice, although this effect was not observed in their younger counterparts. Subsequent investigations focusing on exploring the mechanisms, revealed that repetitive administration of SW033291 effectively mitigated age-induced oxidative stress and curtailed chronic inflammation within the cardiac tissues of aged mice. These pivotal findings establish a solid foundation for contemplating the prospective therapeutic application of SW033291 in addressing age-related heart failure.

01 Feb 2025·Biochemical and Biophysical Research Communications

SW033291 promotes liver regeneration after acetaminophen-induced liver injury in mice

Article

Author: Zhao, Jinlong ; Lü, Guodong ; Jia, Yutong ; Liao, Xia ; Liu, Hui ; Fang, Ziyi ; Li, Jing ; Du, Yun ; Tuniyazi, Xiayidanmu

Acetaminophen (APAP) is a commonly utilized antipyretic and analgesic drug. Overdose of APAP is a primary contributor to drug-induced liver injury and acute liver failure (ALF). SW033291 has been shown to play a role in tissue regeneration in various diseases; however, its potential to facilitate liver regeneration following APAP-induced hepatic injury remains unexamined. Thus, this study focused on exploring the therapeutic impacts and mechanisms of SW033291 on liver damage by establishing models of APAP-induced acute liver injury in mice. The results showed that treatment with SW033291 reduces serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, decreases the area of hepatic necrosis, increases glutathione (GSH) levels, and decreases tissue malondialdehyde (MDA) content, as well as the expression levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in mice with liver injury. It could also promote hepatocyte proliferation and inhibit apoptosis by increasing tissue prostaglandin E2 (PGE2) levels. In conclusion, SW033291 demonstrates the capacity to ameliorate APAP-induced hepatic injury in mice by fostering liver regeneration, attenuating oxidative stress, and modulating inflammatory responses, thereby presenting itself as a promising candidate for the development of therapeutic interventions targeting acute liver failure.

01 Jan 2025·Chemical Engineering Journal

Multifunctional neuroimmunoregulatory nanoenzyme-enhanced hydrogel promotes bone regeneration by improving bone healing microenvironment

Author: Wang, Linnan ; Wang, Lei ; Long, Xingxia ; Yang, Xi ; Zheng, Shuxin ; Li, Qiujiang ; Hu, Bowen ; Deng, Zhipeng ; Zhu, Ce ; Song, Yueming ; Zhang, Zhuang ; Li, Junhu ; Yang, Huiliang

Despite advancements in bone substitute materials for promoting osteogenic activity and angiogenesis, achieving optimal bone regeneration remains challenging due to the complexity of the biol. processes involved.An ideal bone healing strategy should integrate multiple biol. needs in bone microenvironment, such as innervation, immune regulation, angiogenesis and osteogenesis, and achieve dynamic regulation and promote healing through the interaction of osteocytes, osteogenic factors and biomaterials.In the present study, we investigates a bone regeneration strategy based on bioactive glass (BG)-pretreated extracellular vesicles (EVs) encapsulated within a CeO₂-SW033291 (CeO₂-SW) hydrogel.BG stimulation enhances EVs stability and functionality, promoting anti-inflammatory and bone regenerative capabilities.CeO₂ nanoparticles have antioxidant properties and, when combined with SW033291, can increase PGE2 levels to mediate sensory nerves to control bone homeostasis and promote bone healing.The resulting hydrogel, BEV/CeO2-SW@Gel, demonstrates improved biocompatibility, angiogenesis, osteogenic differentiation, and nerve immune regulation both in vitro and in a rat calvarial defect model.RNA sequencing reveals the hydrogel′s potential to activate MAPK signaling, enhancing osteoblast function.These findings suggest BEV/CeO₂-SW@Gel as a promising cell-free therapeutic for bone repair.This study provides a promising biomaterial with potential clin. application for the treatment of critical bone defects in the future.

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