Rat MPO ELISA kit

Traditional ayurvedic medicine, Arjunarishta (AA) is used to treat several inflammatory conditions including dysentery associated with blood. The formulation is a decoction ofTerminalia arjuna(Roxb.) Wight and Arn. (TA),Madhuca indicaJ.F.Gmel.,Vitis viniferaL.,Woodfordia fruticosa(L.) Kurz., andSaccharum officinarumL.Terminalia arjuna, a major constituent of this formulation has been recognized for anti-inflammatory effects. This study aimed at evaluating beneficial effects of AA and probable mechanism of action in Trinitrobenzenesulphonicacid (TNBS) induced colitis model. Response to AA treatment was explored through determination of disease activity index (DAI), histological assessment and damage scores, colonic pro-inflammatory cytokine/chemokine expression and estimation of oxidative stress biomarkers. Improvement in gut microbiome and plasma zinc level was also assessed. Study findings directed therapeutic effects of AA treatment in colitis model by attenuating the colitis symptoms such as weight loss, diarrhoea, blood in stool; histological damage; and downregulated expression of pro-inflammatory cytokines/chemokine (TNF-alpha, IL-1 beta, IL-6) and MCP-1). Similarly reduced oxidative stress by decreased level of Nitric Oxide (NO), Myeloperoxidase (MPO), Malondialdehyde (MDA) and enhanced level of Catalase (CAT), Superoxide dismutase (SOD) and Reduced Glutathione (GSH) was also witnessed. In addition, an improved beneficial fecal microbiome profile and restored plasma zinc status was revealed compared to the TNBS control group. The present study directs that downregulated pro-inflammatory cytokines/chemokine expression, enhancement of antioxidant effect, increased plasma zinc status and promising role in modulating fecal microbiome might be potential mechanisms for the therapeutic effect of AA treatment against colitis.

Purpose Reactive oxygen and nitrogen species (ROS/RNS) production and the NF-kappa B activation are critically involved in inflammatory responses, but knowledge about the temporal dynamics during acute and chronic inflammation is limited. Here, we present a comparative longitudinal in vivo study of both parameters in an experimental model of acute and chronic T cell-driven delayed-type hypersensitivity reaction (DTHR) using noninvasive optical imaging. Procedures Trinitrochlorobenzene (TNCB)-sensitized NF-kappa B-luciferase-reporter and wild-type mice were TNCB challenged on the right ear to elicit acute DTHR and then repetitively challenged (up to five times) to induce chronic DTHR. Mice were treated with the ROS-scavenging and NF-kappa B inhibiting molecule N-acetylcysteine (NAC) or underwent sham treatment. ROS/RNS production was noninvasively analyzed in vivo using the ROS-/RNS-sensitive chemiluminescent probe L-012, and NF-kappa B activation was measured using NF-kappa B-luciferase-reporter mice. H&E staining, CD3 and myeloperoxidase (MPO) immunohistochemistry (IHC), and quantitative PCR (qPCR) analyses were employed to investigate immune cell infiltration and expression of NF-kappa B- and ROS-/RNS-driven genes. Results In acute DTHR, we found strongly elevated ROS/RNS production and NF-kappa B activation 12 h after the 1st TNCB ear challenge, peaking at 24 h after the challenge. In chronic DTHR, ROS production peaked as early as 4 h after the 5th TNCB challenge, whereas NF-kappa B activity peaked after 12 h. The increase in ROS/RNS production in acute DTHR was higher than the increase in NF-kappa B activity but the relationship was inverse in chronic DTHR. Treatment with the ROS scavenger NAC had differential effects on ROS/RNS production and NF-kappa B activation during acute and chronic DTHR. Ex vivo cross-validation by histopathology and qPCR analysis correlated closely with the in vivo imaging results. Conclusions Noninvasive in vivo imaging is capable of assessing the temporal dynamics of ROS/RNS production and NF-kappa B activation during progression from acute to chronic DTHR and enables monitoring of anti-inflammatory treatment responses.