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Controlled Inflammation Drives Neutrophil-Mediated Precision Drug Delivery in Heterogeneous Tumors.
Adv Sci (Weinh)
January 2025
Department of Radiology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, P. R. China.
Tumor heterogeneity remains a formidable obstacle in targeted cancer therapy, often leading to suboptimal treatment outcomes. This study presents an innovative approach that harnesses controlled inflammation to guide neutrophil-mediated drug delivery, effectively overcoming the limitations imposed by tumor heterogeneity. By inducing localized inflammation within tumors using lipopolysaccharide, it significantly amplify the recruitment of drug-laden neutrophils to tumor sites, irrespective of specific tumor markers.
View Article and Find Full Text PDFInhibition of RIPK1-driven necroptosis ameliorates inflammatory hyperalgesia caused by lipopolysaccharide: involvement of TLR-, NLRP3-, and caspase-11-mediated signaling pathways.
Cell Mol Biol (Noisy-le-grand)
January 2025
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Türkiye.
Increasing evidence suggests that inhibition of receptor-interacting serine/threonine-protein kinase (RIPK) 1/RIPK3/mixed lineage kinase domain-like pseudokinase (MLKL) necrosome has protective effects in vivo models of painful conditions seen in humans associated with inflammation and demyelination in the central nervous system. However, the contribution of RIPK1-driven necroptosis to inflammatory pain remains unknown. Therefore, this study aims to determine the effect of necrostatin (Nec) -1s, a selective RIPK1 inhibitor, on lipopolysaccharide (LPS)-induced inflammatory pain and related underlying mechanisms.
View Article and Find Full Text PDFDipyridamole Attenuates Experimental Periodontitis by Regulating M1 Macrophage Polarization via PKA/PKG Pathways.
J Periodontal Res
January 2025
Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, China.
Aim: Periodontitis is a chronic inflammatory disease initiated by dysbiosis of the local microbial community. As a non-specific phosphodiesterase inhibitor, dipyridamole features anti-oxidant and anti-inflammatory properties. This study aimed to investigate the effects of dipyridamole in an experimental rat model of periodontitis.
View Article and Find Full Text PDFPreparation and stability of chebulagic acid and chebulinic acid from Terminalia chebula and their biological activity.
Pak J Pharm Sci
January 2025
College of Pharmacy, Liaoning University of Traditional Chinese Medicine, Dalian, China/Province Multi-Component Chinese Medicine Engineering Technology Research Center of Liaoning, Dalian, China/Modern Traditional Chinese Medicine Research and Engineering Laboratory of Liaoning, Dalian, China.
Chebulagic acid and chebulinic acid are the two tannin compounds with the highest content in Terminalia chebula, they were separated by ODS column eluted with 20% methanol and 35% methanol, respectively. The compounds were identified by comparing the data of H NMR and C NMR with the literature; HPLC method was used to investigate the stable storage conditions of chebulagic acid and chebulinic acid; lipopolysaccharide (LPS) induced in vivo inflammation model and RAW264.7 macrophage in vitro inflammatory model to evaluate the anti-inflammatory activities of chebulagic acid and chebulinic acid.
View Article and Find Full Text PDF[Research advances in the mechanism of Toll-like receptor 4 mediated intestinal injury and inflammatory response in necrotizing enterocolitis].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
Department of Neonatology, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200062, China. *Corresponding author, E-mail:
Necrotizing enterocolitis (NEC) is an intestinal inflammatory and necrotic disease seen in premature infants, and remains the leading cause of death resulted from gastrointestinal diseases in premature infants. The specific pathogenesis of NEC is still unclear. In recent years, a lot of studies have reported that Toll-like receptor 4 (TLR4) plays a key role in the pathogenesis of NEC.
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