APicrorhiza kurroaDerivative, Picroliv, Attenuates the Development of Dextran-Sulfate-Sodium-Induced Colitis in Mice

Abstract

Background. Free radicals and proinflammatory cytokines have been shown to play a critical role in the pathogenesis of ulcerative colitis (UC). Picroliv, a Picrorhiza kurroa derivative, has been demonstrated to have antioxidant and anti-inflammatory effect. The purpose of the study was to investigate the effects of picroliv on experimental model of UC in mice. Materials and Methods. Picroliv was administrated orally by gavage to mice with colitis induced by dextran sulfate sodium (DSS). Disease activity index (DAI), colon length, and histology score were observed. Myeloperoxidase (MPO) activity, and SOD, MDA concentrations were measured by enzyme-linked immunosorbent assay (ELISA) while the expression of cytokine mRNAs was studied by real-time-quantitative polymerase chain reaction and also ELISA. The expression of NF-κB p65 was observed by immunohistochemistry staining and western blotting. Results. A significant improvement was observed in DAI and histological score in mice treated with picroliv, and incerased MPO activity, MDA concentrations, and the expression of IL-1β, TNF-α, and NF-κB p65 in mice with DSS-induced colitis were significantly reduced while decreased SOD level increased following administration of picroliv. Conclusion. The administration of picroliv leads to an amelioration of DSS-induced colitis, suggesting administration of picroliv may provide a therapeutic approach for UC.

Ursolic acid protects against ulcerative colitis via anti-inflammatory and antioxidant effects in mice

“…These results suggested that antioxidative protection may be an important mechanism for UA in colitis. Furthermore, the accumulation of ROS in colon tissues, in addition to directly damaging intestinal epithelial cells, stimulates inflammatory responses to release pro-inflammatory cytokines, particularly TNF-α and IL-1β (28,29), which may cause further damage.…”

Phytochemicals in Wound Healing

“…Picroliv treatment not only enhanced the sprouting and migration of endothelial cells but also showed improved re-epithelialization, neovascularization, and migration of various cells such as endothelial, dermal myofibroblasts and fibroblasts into the wound bed. 49 In rats, picroliv also up-regulated the expression of VEGF in human umbilical vein endothelial cells and insulin-like growth factor during hypoxia. 51 The exact mechanism of action of the therapeutic action of picroliv is unclear.…”

“…3. 49,50 Picroliv in wound healing and angiogenesis Singh et al investigated the effect and role of picroliv in an ex vivo rat aorta ring model of angiogenesis and punch wound healing. Picroliv treatment not only enhanced the sprouting and migration of endothelial cells but also showed improved re-epithelialization, neovascularization, and migration of various cells such as endothelial, dermal myofibroblasts and fibroblasts into the wound bed.…”

“…Chemical structure of picroliv and its constituents. 49,50 re-epithelialization of the wounds. 52 The increase in the synthesis of collagen, fibronectin, and TGF-1 was also reported by Sidhu et al in arnebin-1-treated wounds compared with the untreated control.…”

Biosynthesis and therapeutic implications of iridoid glycosides from Picrorhiza genus: the road ahead

“…Moreover, the optimization of therapeutic dose and time window of P-II revealed that 20 mg/kg body weight P-II should be injected intraperitoneally at ischemia 1.5 h in treating cerebral ischemic injury (Pei et al 2012). Further treatment with 10-20 mg/kg body weight P-II at ischemia 1.5 h recorded the reduced levels of free radicals in cerebral ischemic injury along with the reduction in malonaldehyde Anti-allergic and anti-anaphylactic 6.25-25 mg/kg for 4 days, oral In vivo Kutkin Baruah et al 1998 12 Ulcerative colitis 12.5 mg/kg for 7 days, oral In vivo Kutkin Zhang et al 2012 content and an improvement in superoxide dismutase activity (Zhang et al 2013). This suggests that antioxidant potential of P-II could reduce the oxidative damage induced by cerebral ischemic injury.…”