Anti‐Inflammatory Effect of Erythropoietin in the TNBS‐induced Colitis

Abstract

Erythropoietin is a potent stimulator of erythroid progenitor cells, which is able to inhibit NF-kB activation, due to its pleiotropic properties, thus promoting an anti-inflammatory effect. As inflammatory bowel disease is a chronic disease with reduced quality of life, and the current pharmacotherapy only induces or maintains the patient in remission, there is a crucial need of new pharmacological approaches. The main objective of this study was to evaluate the effect of erythropoietin in the TNBS-induced colitis model in mice with a normal intestinal flora. Mice with TNBS-induced colitis were treated with a daily dose of erythropoietin at 500 IU/kg bw/day and 1000 IU/Kg bw/day IP during 4 days. As to clinical symptoms/signs, erythropoietin attenuated the decreased body-weight and reduced diarrhoea and oedema of the anus registered in the non-treated mice group in a dose-dependent manner. The anti-inflammatory properties of erythropoietin in the TNBS-induced colitis were confirmed by suppression of pro-inflammatory mediators, such as TNF-α, IL-1β and MPO, as well as a significant increase in the anti-inflammatory cytokine, IL-10, was promoted. These treated mice also presented a reduction in haemoglobin faecal and ALP, suggesting a beneficial effect of erythropoietin in the haemorrhagic focus and destruction of the enterocyte associated with the colon injury induced by TNBS, respectively. The histopathological score was reduced after treatment with erythropoietin, decreasing the severity and extension of the colitis. Furthermore, renal and hepatic biomarkers, as well as haematocrit concentration, remained stabilized after treatment. In conclusion, erythropoietin reduces the inflammatory response associated with TNBS-induced colitis in mice.

Polydatin reduces Staphylococcus aureus lipoteichoic acid‐induced injury by attenuating reactive oxygen species generation and TLR2‐NFκB signalling

“…Therefore, in this study, we used macrophages instead of primary endometrial epithelial cells to explore the underlying mechanism of PD, which could have more general applicability—that is, PD may also play a similar role in other inflammatory diseases that have been confirmed in our previous studies . In this research, we evaluated the protective effects of PD in vivo using histological analyses, including H&E, immunofluorescence staining of phosphorylated NF‐κB involved in the regulation of the inflammatory process and the TUNEL assay as well as some of the crucial apoptosis‐related proteins. All of the in vivo experiments showed that PD can ameliorate the pathological conditions and attenuate the phosphorylation of NF‐κB and anti‐apoptotic effect, indicating that PD may have potential anti‐inflammatory and anti‐apoptotic effects in LTA‐induced injury in vivo .…”

Thiadiazolidinone-8 Ameliorates Inflammation Associated with Experimental Colitis in Mice

“…TNBS was instilled as an intracolonic single dose as previously described by Mateus et al [13]. Briefly, mice were left unfed during 24 h. In the induction day (day 0), mice were anesthetized with ketamine 100 mg/kg + xylazine 10 mg/kg.…”

Curcumin attenuates erythropoiesis in recombinant human erythropoietin-induced polycythemia in rats

“…[1] Shin and Cho suggested a novel strategy of EPO and granulocyte colony-stimulating factor combination therapy for stroke patients in their exploratory study. [2] In addition, EPO had a neuroprotective role in rotenoneinduced parkinsonism in rats, [3] an anti-inflammatory effect in the development of experimental colitis, [4] and a role in the regulation of body weight, fat mass, and glucose metabolism. [5] On the other hand, there is an increased mortality rate with recombinant human EPO treatment in stroke patients due to the toxicity of the high dose of EPO, this toxicity may partially result from increased hematocrit (Hct)-associated side effects, such as hypertension and thromboembolism.…”