Sonodynamic therapy (SDT) induces reactive oxygen species (ROS) to kill tumor cells. Heme oxygenase-1 (HO-1), as an important antioxidant enzyme, resists killing by scavenging ROS. Zinc protoporphyrin (ZnPP) not only effectively inhibits HO-1 activity, but also becomes a potential sonosensitizer. However, its poor water solubility limits its applications. Herein, we developed an improved water-soluble method. It was proved that pegylated zinc protoporphyrin-mediated SDT (PEG-ZnPP-SDT) could significantly enhance ROS production by destroying the HO-1 antioxidant system in ovarian cancer. Increased ROS could cause mitochondrial membrane potential collapse, release cytochrome c from mitochondria to the cytoplasm, and trigger the mitochondrial-caspase apoptotic pathway. In conclusion, our results demonstrated that PEG-ZnPP-SDT, as a novel sonosensitizer, could improve the antitumor effects by destroying the HO-1 antioxidant system. It provided a new therapeutic strategy for SDT to treat cancers, especially those with higher HO-1 expression.
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http://dx.doi.org/10.3390/pharmaceutics15092275 | DOI Listing |
J Trauma Acute Care Surg
January 2025
From the Division of Gastrointestinal, Trauma, and Endocrine Surgery, Department of Surgery (A.P., K.M.M., A.C.Q., E.J.K., J.-P.I.), Division of Burn Research (E.J.K.), and Division of Alcohol Research (E.J.K.), Department of Immunology and Microbiology, University of Colorado, Aurora, Colorado.
Background: Burn injuries trigger a systemic hyperinflammatory response, leading to multiple organ dysfunction, including significant hepatic damage. The liver plays a crucial role in regulating immune responses and metabolism after burn injuries, making it critical to develop strategies to mitigate hepatic impairment. This study investigates the role of methylation-controlled J protein (MCJ), an inner mitochondrial protein that represses complex I in burn-induced oxidative stress and mitochondrial dysfunction, using an in vitro Alpha Mouse Liver 12 cell model.
View Article and Find Full Text PDFBioact Mater
April 2025
School of Biomedical Engineering, Anhui Provincial Institute of Translational Medicine, Anhui Engineering Research Center for Medical Micro-Nano Devices, Anhui Medical University, Hefei, 230011, PR China.
Oxidative stress, dysbiosis, and immune dysregulation have been confirmed to play pivotal roles in the complex pathogenesis of inflammatory bowel disease (IBD). Herein, we design copper ion-luteolin nanocomplexes (CuL NCs) through a metal-polyphenol coordination strategy, which plays a multifaceted role in the amelioration of IBD. The fabricated CuL NCs function as therapeutic agents with exceptional antioxidant and anti-inflammatory capabilities because of their great stability and capacity to scavenge reactive oxygen species (ROS).
View Article and Find Full Text PDFHeliyon
December 2024
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 22452, Riyadh, 11495, Saudi Arabia.
Background: Purpose: Valproate (VPA) is an antiepileptic drug widely used to treat various psychiatric and neurological disorders. Although its use is generally considered safe, chronic administration may lead to kidney injury. The mechanisms underlying VPA kidney toxicity are not entirely explored.
View Article and Find Full Text PDFCurr Mol Med
January 2025
Department of Ophthalmology, Hebei Medical University, Shijiazhuag 050017, Hebei, China.
Purpose: To investigate the effect of the SUMOylation inhibitor TAK981 on hydrogen peroxide (H2O2)-induced oxidative damage in human retinal pigment epithelial cells (ARPE-19) and its regulatory mechanism.
Methods: An oxidative damage model of ARPE-19 cells induced by H2O2 was established, and 1, 2, and 5 µM TAK981 solutions were administered for intervention respectively. Normal cells were used as the control group.
Inflammopharmacology
January 2025
General Surgery Department, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China.
Background: Ulcerative colitis (UC) is a significant inflammatory bowel disease (IBD) that typically arises from chronic inflammation of the intestinal tract. Report suggest that anti-inflammatory drug plays a crucial role in the protection of UC. The recent study demonstrated that columbianadin has a protective effect against UC induced by dextran sulfate sodium (DSS) in rats through the modulation of HO-1/Nrf2 and TLR4-NF-κB signaling pathways.
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