Zinc l-carnosine protects colonic mucosal injury through induction of heat shock protein 72 and suppression of NF-κB activation

Reduced Hsp70 and Glutamine in Pediatric Severe Malaria Anemia: Role of hemozoin in Suppressing Hsp70 and NF-κB Activation

“…Accumulating evidence suggests that the protective (antiinflammatory) role of Hsp70 is mediated through downregulation of NF-κB, since NF-κB activation and translocation into the nucleus promotes elevated proinflammatory mediators (14,(16)(17)(18)(19)(20)(21)41,50,72,73). Consistent with this notion, we and others have demonstrated that overexpression of Hsp70 protein blocks nuclear translocation of NF-κB and thereby reduces proinflammatory mediator production (19)(20)(21)50).…”

Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota

“…155 Zinc-L-carnosine complex was found to increase iHSP70, to suppress NF-jB activation, and, finally, to protect rats submitted to chemically induced (acetic acid) colonic mucosa injury. 147 This was due to the zinc itself, potentiated by the presence of L-carnosine, because zinc sulfate, on a molar basis, displayed a lower effect, while L-carnosine alone had no effect at all. 147 Zinc-mediated protection through iHSP induction was also observed in the colon of mice submitted to dextran sulfate sodium-induced colitis and supplemented (or not) with polaprezinc (15 mg/kg body weight) or zinc sulfate (7.5 mg/kg) for 7 days.…”

“…Finally, neither human colostrum proteins nor b-alanyl-histidine dipeptide (L-carnosine) influenced iHSP70 in IEC-6 cells or in rats submitted to acetic acid-induced colonic mucosa injury, respectively. 134,147 Plant products. Kidney bean (Phaseolus vulgaris) phytohemagglutinin and germ agglutinin from wheat grain (Triticum aestivum) are known as toxic compounds.…”

Diabetic Nephropathy: Current and Novel Therapeutic Approaches to Prevent Its Development and Progression

“…Indeed, our group has demonstrated the importance of NF-B in the pathogenesis of early renal macrophage infiltration in experimental diabetes, which could be modulated by interruption of the RAS (Lee, Cao et al 2004;Liu, Wei et al 2006). Moreover, diabetes-induced increases in NF-B activation are prevented by numerous therapeutics including Metformin (Isoda, Young et al 2006) aspirin (Zheng, Howell et al 2007) Vitamin B derivatives (Hammes, Du et al 2003) carnosine (Odashima, Otaka et al 2006) and thiazolidinediones (Marx, Walcher et al 2004). It is possible that NF-B, like PKC, is a central mediator which drives the downstream pathogenic consequences of interactions between hemodynamic and glucose dependent pathways in diabetic vascular complications.…”