TNF/TNFR1 pathway and endoplasmic reticulum stress are involved in ofloxacin-induced apoptosis of juvenile canine chondrocytes

Cytotoxicity of atropine to human corneal epithelial cells by inducing cell cycle arrest and mitochondrion-dependent apoptosis

“…We found that atropine could induce the activation of caspase-2, -9 and -3 hierarchically in HCEP cells. Since caspase-2 is an important regulator of tumor necrosis factor receptor 1 (TNFR1)-mediated extrinsic apoptotic pathway while caspase-9 is a key regulator of the mitochondriondependent intrinsic apoptotic pathway (Fan et al, 2005;Zhang et al, 2014), the activation of both caspase-2 and -9 imply that the atropine-induced apoptosis in HCEP cells might be regulated by a TNFR1-mediated mitochondrion-dependent pathway. The involvement of both an extrinsic death receptor-mediated and an intrinsic mitochondrion-dependent signaling pathways has also been reported in the apoptosis induced by other chemotherapeutic agents (Sun et al, 1999;Yu et al, 2014;Zhang et al, 2014).…”

Synthesis, characterization and DNA-binding properties of Ru(II) complexes coordinated by ofloxacin as potential antitumor agents

“…The use of ofloxacin for urinary tract infection treatment has increased in the past decade because this antibiotic has excellent efficacy and increases resistance to older agents, such as trimethoprim and sulfamethoxazole [7]. Some studies have reported that ofloxacin could efficiently inhibit the growth of various tumor cells via induced apoptosis [8,9]. Considerable evidence suggests that ruthenium(II)-polypyridyl complexes can kill tumor cells by interacting with DNA and inducing apoptosis [10][11][12].…”

Inhibitor of Apoptosis Proteins (IAPs) Limit RIPK1-Mediated Skin Inflammation

“…SM-induced keratinocyte apoptosis is almost abolished in the Ripk1 heterozygote and FasL gld/gld mice, implying that activity of this caspase-8 complex is the cause of keratinocyte death. Some clinical drugs causing TEN are also able to promote formation of a caspase-8econtaining complex (Fecker et al, 2010;Jun et al, 2003;Yadav et al, 2015;Yasuda et al, 2008;Zhang et al, 2014), In particular, nonsteroidal anti-inflammatory drugs are known to do so in a SMAC/Diablo-dependent manner (Kohli et al, 2004;Qiu et al, 2010). It is therefore conceivable that drug-induced TEN is driven by activated RIPK1 and that RIPK1 might be a therapeutic target for TEN.…”