Anti-Myeloperoxidase monoclonal antibody, clone O5D8 [HRP]

Gastric ulcer is a prevalent disease with various etiologies, including non-steroidal anti-inflammatory drugs (NSAIDs), stress conditions, and alcohol, resulting in an inflammatory condition in the gastric mucosa. The aim of this study was to explore the protective effects of modafinil on gastric erosions induced by indomethacin, water-immersion stress, and alcohol in rats and to evaluate the role of nitric oxide (NO) pathway. Animals were allocated to the three experimental models of gastric ulcer - indomethacin (30 mg/kg PO), water-immersion stress, and ethanol (5 ml/kg PO). Induction of gastric ulcer in all models caused an increase in J-score (macroscopic assessment), biochemical markers, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1 beta), and myeloperoxidase (MPO), and microscopic destructions. Administration of modafinil (50 and 100 mg/kg i. p) significantly improved J-score in the indomethacin (P < 0.05) and stress models (P < 0.001). Moreover, the level of TNF-alpha IL-1 beta, and MPO was deceased after modafinil administration (P < 0.001). However, modafinil did not have any effects on gastric injury induced by ethanol. In addition, co-administration of L-NAME (a non-specific NO synthase inhibitor) and aminoguanidine (an inducible NO synthase inhibitor) with modafinil significantly neutralized the gastroprotective effect of modafinil in the indomethacin and water-immersion stress groups (P < 0.05, and P < 0.01; respectively), while 7-nitroindazole (a neuronal NO synthase inhibitor) did not show such reversing effects. In conclusion, modafinil possesses gastroprotective effects on the gastric lesions induced by indomethacin and stress, which are probably mediated via the inflammation inhibition and NO pathway modulation.

Escherichia coli(E. coli) infection is very common among young growing animals, and zinc supplementation is often used to alleviate inflammation induced by this disease. Therefore, the objective of this study was to evaluate whether chitosan-chelated zinc (CS-Zn) supplementation could attenuate gut injury induced byE. colichallenge and to explore how CS-Zn modulates cecal microbiota and alleviates intestinal inflammation in weaned rats challenged withE. coli.36 weaned rats (55.65 +/- 2.18 g of BW, n = 12) were divided into three treatment groups consisting of unchallenged rats fed a basal diet (Control) and two groups of rats challenged withE. coliand fed a basal diet or a diet containing 640 mg/kg CS-Zn (E.coli+ CS-Zn, containing 50 mg/kg Zn) for a 14-day experiment. On days 10 to 12, each rat was given 4 ml ofE. colisolution with a total bacteria count of 10(10)CFU by oral gavage daily or normal saline of equal dosage. CS-Zn supplementation mitigated intestinal morphology impairment (e.g. higher crypt depth and lower macroscopic damage index) induced byE. colichallenge (P< 0.05), and alleviated the increase of Myeloperoxidase (MPO) activity afterE. colichallenge (P < 0.05). 16S rRNA sequencing analyses revealed thatE. colichallenge significantly increased the abundance of Verrucomicrobia andE. coli(P< 0.05). However, CS-Zn supplementation increased the abundance ofLactobacillusand decreased the relative abundance of Proteobacteria,DesulfovibrioandE. coli (P< 0.05). The concentrations of butyrate in the cecal digesta, which decreased due to the challenge, were higher in theE. coli+ CS-Zn group (P< 0.05). In addition, CS-Zn supplementation significantly prevented the elevation of pro-inflammatory cytokines IL-6 concentration and up-regulated the level of anti-inflammatory cytokines IL-10 in cecal mucosa induced byE. coliinfection (P< 0.05). In conclusion, these results indicate that CS-Zn produces beneficial effects in alleviating gut mucosal injury ofE. colichallenged rats by enhancing the intestinal morphology and modulating cecal bacterial composition, as well as attenuating inflammatory response.