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Osteomyelitis is a well-known bone infection in humans. The primary symptoms are fever, pain, weakness, and redness of the bone. l-Homocarnosine is a bioactive peptide abundant in brain and skeletal muscles. The present study evaluated the synergistic effect of vancomycin and l-homocarnosine against osteomyelitis in the Staphylococcus aureus-induced rat model of osteomyelitis. Animals were classified into the following groups: sham (group I), osteomyelitis (group II, control), vancomycin (25 mg/kg body weight, group III), l-homobrassinolide (25 mg/kg body weight, group IV), and vancomycin (25 mg/kg body weight) + l-homobrassinolide (25 mg/kg body weight) (group V). Lipid peroxidation, superoxide dismutase (SOD), glutathione peroxidase (Gpx), catalase, reduced glutathione (GSH), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were determined. Assessments of bacterial growth and histopathological analyses were carried out. Lipid peroxidation, GSH, SOD, catalase, and Gpx levels recovered to near normal levels with the combined treatment of vancomycin and l-homocarnosine. TNF-α and IL-6 levels were reduced to near normal levels. Combined supplementation of vancomycin and l-homocarnosine reduced bacterial growth in bone and wire. Furthermore, bone infections and histopathological scores were also reduced. In summary, we showed that combined treatment of vancomycin and l-homocarnosine was more effective against bacterial growth and bone infection compared to monotherapy with vancomycin or l-homocarnosine.

Graphical abstract Highlights • Vancomycin and l -homocarnosine reduced lipid peroxidation and TNF-α & IL-6. • Vancomycin and l -homocarnosine reduced bacterial growth and bone infection. • Vancomycin and l -homocarnosine reduced histopathological score. • Vancomycin and l -homocarnosine increased GSH, Gpx, catalase and SOD. Abstract Osteomyelitis is a well-known bone infection in humans. The primary symptoms are fever, pain, weakness, and redness of the bone. l -Homocarnosine is a bioactive peptide abundant in brain and skeletal muscles. The present study evaluated the synergistic effect of vancomycin and l -homocarnosine against osteomyelitis in the Staphylococcus aureus -induced rat model of osteomyelitis. Animals were classified into the following groups: sham (group I), osteomyelitis (group II, control), vancomycin (25 mg/kg body weight, group III), l -homobrassinolide (25 mg/kg body weight, group IV), and vancomycin (25 mg/kg body weight) + l -homobrassinolide (25 mg/kg body weight) (group V). Lipid peroxidation, superoxide dismutase (SOD), glutathione peroxidase (Gpx), catalase, reduced glutathione (GSH), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were determined. Assessments of bacterial growth and histopathological analyses were carried out. Lipid peroxidation, GSH, SOD, catalase, and Gpx levels recovered to near normal levels with the combined treatment of vancomycin and l -homocarnosine. TNF-α and IL-6 levels were reduced to near normal levels. Combined supplementation of vancomycin and l -homocarnosine reduced bacterial growth in bone and wire. Furthermore, bone infections and histopathological scores were also reduced. In summary, we showed that combined treatment of vancomycin and l -homocarnosine was more effective against bacterial growth and bone infection compared to monotherapy with vancomycin or l -homocarnosine. [ABSTRACT FROM AUTHOR]

We investigated the therapeutic effects of l-homocarnosine against inflammation in a rat model of cerebral ischemia-reperfusion injury. Rats were grouped into control, middle cerebral artery occlusion (MCAO), 0.5 mM l-homocarnosine + MCAO, and 1 mM l-homocarnosine + MCAO treatment groups. Superoxide dismutase (SOD), glutathione peroxidase (Gpx), catalase, lipid peroxidation, and reduced glutathione (GSH) levels were measured. Neurological scores were assessed, and histopathology, scanning electron microscopy (SEM), and fluorescence microscopy analyses were conducted. The mRNA expression levels of nod-like receptor protein 3 (NLRP3), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) and protein expression levels of NLRP3 were assessed. l-Homocarnosine supplementation substantially increased SOD, catalase, Gpx, and GSH levels, whereas it reduced the levels of lipid peroxidation relative to MCAO rats. l-Homocarnosine significantly reduced the infarct area and neurological deficit score, as well as histopathological alteration, apoptosis, and necrosis in brain tissue. The mRNA expression levels of NLRP3, TNF-α, and IL-6 were increased in MCAO rats, whereas l-homocarnosine supplementation reduced mRNA expression by >40%, and NLRP3 protein expression was reduced by >30% in 1 mM l-homocarnosine-treated MCAO rats. We propose that l-homocarnosine exerts a protective effect in cerebral ischemia-reperfusion injury-induced rats by downregulating NLRP3 expression., (Copyright © 2018 Elsevier B.V. All rights reserved.)