Effect of thermophilic bacterium HB27 manganese superoxide dismutase in a rat model of chronic prostatitis/chronic pelvic pain syndrome(CP/CPPS)

We investigated the therapeutic effects of superoxide dismutase(SOD)from thermophilic bacterium HB27 on chronic prostatitis/chronic pelvic pain syndrome(CP/CPPS)and its underlying mechanisms.A Sprague–Dawley rat model of CP/CPPS was prepared and then administered saline or Thermus thermophilic(Tt)-SOD intragastrically for 4 weeks.Prostate inflammation and fibrosis were analyzed by hematoxylin and eosin staining,and Masson staining.Alanine transaminase(ALT),aspartate transaminase(AST),serum creatinine(CR),and blood urea nitrogen(BUN)levels were assayed for all animals.Enzyme-linked immunosorbent assays(ELISA)were performed to analyze serum cytokine concentrations and tissue levels of malondialdehyde,nitric oxide,SOD,catalase,and glutathione peroxidase.Reactive oxygen species levels were detected using dichlorofluorescein diacetate.The messenger ribonucleic acid(mRNA)expression of tissue cytokines was analyzed by reverse transcription polymerase chain reaction(RT-PCR),and infiltrating inflammatory cells were examined using immunohistochemistry.Nuclear factor-κB(NF-κB)P65,P38,and inhibitor of nuclear factor-κBα(I-κBα)protein levels were determined using western blot.Tt-SOD significantly improved histopathological changes in CP/CPPS,reduced inflammatory cell infiltration and fibrosis,increased pain threshold,and reduced the prostate index.Tt-SOD treatment showed no significant effect on ALT,AST,CR,or BUN levels.Furthermore,Tt-SOD reduced inflammatory cytokine expression in prostate tissue and increased antioxidant capacity.This anti-inflammatory activity correlated with decreases in the abundance of cluster of differentiation 3(CD3),cluster of differentiation 45(CD45),and macrophage inflammatory protein 1α(MIP1α)cells.Tt-SOD alleviated inflammation and oxidative stress by reducing NF-κB P65 and P38 protein levels and increasing I-κBαprotein levels.These findings support Tt-SOD as a potential drug for CP/CPPS.

Ccrl2 deficiency deteriorates obesity and insulin resistance through increasing adipose tissue macrophages infiltration

Obesity-induced inflammation,characterized by augmented infiltration and altered balance of macrophages,is a critical component of systemic insulin resistance.Chemokine-chemokine receptor system plays a vital role in the macrophages accumulation.CC-Chemokine Receptor-like 2(Ccrl2)is one of the receptors of Chemerin,which is a member of atypical chemokine receptors(ACKR)family,reported taking part in host immune responses and inflammation-related conditions.In our study,we found ccrl2 expression significantly elevated in visceral adipose tissue(VAT)of high fat diet(HFD)induced obese mice and ob/ob mice.Systemic deletion of Ccrl2 gene aggravated HFD induced obesity and insulin resistance and ccrl2−/−mice showed aggravated VAT inflammation and increased M1/M2 macrophages ratio,which is due to the increase of macrophages chemotaxis in Ccrl2 deficiency mice.Cumulatively,these results indicate that Ccrl2 has a critical function in obesity and obesity-induced insulin resistance via mediating macrophages chemotaxis.