Search results for: Polaprezinc

Authors: Gaweł Magdalena, Lipkowska Anna, Olbert Magdalena, Frąckiewicz Ewelina, Librowski Tadeusz, Nowak Gabriel, Pilc Andrzej

Abstract:

Heme oxygenase-1 (HO-1), also known as heat shock protein 32 (HSP32), has been shown to be implicated in cytoprotection in various organs. Its activation plays a significant role in acute and chronic inflammation, protecting cells from oxidative injury and apoptosis. This inducible isoform of HO catalyzes the first and rate-limiting step in heme degradation to produce equimolar quantities of biologically active products: carbon monoxide (CO), free iron and biliverdin. CO has been reported to possess anti-apoptotic properties. Moreover, it inhibits the production of proinflammatory cytokines and stimulates the synthesis of the anti-inflammatory interleukin-10 (IL-10), as well as promotes vasodilatation at sites of inflammation. The second product of catalytic HO-1 activity, free cytotoxic iron, is promptly sequestered into the iron storage protein ferritin, which lowers the pro-oxidant state of the cell. The third product, biliverdin, is subsequently converted by biliverdin reductase into the bile pigment bilirubin, the most potent endogenous antioxidant among the constituents of human serum, which modulates immune effector functions and suppresses inflammatory response. Furthermore, being one of the so-called stress proteins, HO-1 adaptively responds to different stressors, such as reactive oxygen species (ROS), inflammatory cytokines and heavy metals and thus protects cells against such conditions as ischemia, hemorrhagic shock, heat shock or hypoxia. It is suggested that pharmacologic modulation of HO-1 may represent an effective strategy for prevention of stress and drug-induced gastrointestinal toxicity. HO-1 is constitutively expressed in normal gastric, intestinal and colonic mucosa and up-regulated during inflammation. It has been proven that HO-1 up-regulated by hemin, heme and cobalt-protoporphyrin ameliorates experimental colitis. In addition, the up-regulation of HO-1 partially explains the mechanism of action of 5-aminosalicylic acid (5-ASA), which is used clinically as an anti-colitis agent. In 2009 Ueda et al. has reported for the first time that mucosal protection by Polaprezinc, a chelate compound of zinc and L-carnosine used as an anti-ulcer drug in Japan, is also attributed to induction of HO-1 in the stomach. Since then, inducers of HO-1 are desired subject of research, as they may constitute therapeutically effective anti-ulcer drugs.

Keywords: heme oxygenase-1, gastric lesions, gastroprotection, Polaprezinc

Procedia PDF Downloads 486

Authors: Boshra Mozaffar, Arash Ardavani, Iskandar Idris

Abstract:

Food taste and flavor affect food choice and acceptance, which are essential to maintain good health and quality of life. Reduced circulating zinc levels have been shown to adversely affect taste which can result in reduced appetite, weight loss and psychological problems, but the efficacy of Zinc supplementation to treat disorders of taste remains unclear. In this systematic review and meta-analysis, we aimed to examine the efficacy of zinc supplementation in the treatment of taste disorders. We searched four electronic bibliographical databases; Ovid MEDLINE, Ovid Embase, Ovid AMAD and PubMed. Article bibliographies were also searched, which yielded additional relevant studies. To facilitate the collection and identification of all available and relevant articles published before 7 December 2020, there were no restrictions on the publication date. We performed a systematic review and meta-analysis according to the PRISMA Statement. This review was registered at PROSPERO and given the identification number CRD42021228461. In total, we included 12 randomized controlled trials with 938 subjects. Intervention includes zinc (sulfate, gluconate, picolinate, polaprezinc and acetate); the pooled results of the meta-analysis indicate that improvements in taste disorder occurred more frequently in the intervention group compared to the control group (RR = 1.8; 95% CI:1.27 -2.57, p=0.009). The doses are equivalent to 17 mg- 86.7 mg of elemental zin for three to six months. Zinc supplementation is an effective treatment for taste disorders in patients with zinc deficiency or idiopathic taste disorders when given in high doses ranging from 68–86.7 mg/d for up to three months. However, we did not find sufficient evidence to determine the effectiveness of zinc supplementation in patients with taste disorders induced by chronic renal failure.

Keywords: taste change, taste disorder, zinc, zinc sulfate or Zn, deficiency, supplementation.

Procedia PDF Downloads 248