8
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Effects of crocin on spatial or aversive learning and memory impairments induced by lipopolysaccharide in rats

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective:

          Neuroinflammation and oxidative stress play essential roles in the pathogenesis and progression of neurodegenerative diseases, such as Alzheimer’s disease. Crocin, main active constituent of Crocus sativus L. (saffron), possesses anti-inflammatory, anti-apoptotic and anti-oxidative capacity. The aim of the present study was to investigate the neuroprotective effect of crocin on lipopolysaccharide (LPS)-induced learning and memory deficits and neuroinflammation in rats.

          Materials and Methods:

          The animals were randomly classified into four groups, including control, LPS, crocin 50 and crocin 100. The rats were treated with either crocin (50 and 100 mg/kg) or saline for a week. Later, LPS (1 mg/kg, i.p.) or saline was administered, and treatments with crocin or saline were continued for 3 more weeks. The behavioral tasks for spatial and aversive memories were performed by the Morris water maze and passive avoidance tasks from post-injection days 18 to 24. Furthermore, the levels of interleukine-1β, lipid peroxidation and total thiol were assayed in the hippocampus and cerebral cortex.

          Results:

          Our results demonstrated that treatment of LPS-treated rats with crocin decreased the escape latency in the Morris water maze and increased the time spent in the target quadrant in the probe trial. Moreover, crocin increased step-through latency in the passive avoidance test. However, there was no significant difference in the oxidative and neuroinflammatory responses among the experimental groups.

          Conclusion:

          Pretreatment with crocin attenuates spatial or aversive learning and memory deficits in LPS-treated rats.

          Related collections

          Most cited references67

          • Record: found
          • Abstract: found
          • Article: not found

          Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration.

          Inflammation is implicated in the progressive nature of neurodegenerative diseases, such as Parkinson's disease, but the mechanisms are poorly understood. A single systemic lipopolysaccharide (LPS, 5 mg/kg, i.p.) or tumor necrosis factor alpha (TNFalpha, 0.25 mg/kg, i.p.) injection was administered in adult wild-type mice and in mice lacking TNFalpha receptors (TNF R1/R2(-/-)) to discern the mechanisms of inflammation transfer from the periphery to the brain and the neurodegenerative consequences. Systemic LPS administration resulted in rapid brain TNFalpha increase that remained elevated for 10 months, while peripheral TNFalpha (serum and liver) had subsided by 9 h (serum) and 1 week (liver). Systemic TNFalpha and LPS administration activated microglia and increased expression of brain pro-inflammatory factors (i.e., TNFalpha, MCP-1, IL-1beta, and NF-kappaB p65) in wild-type mice, but not in TNF R1/R2(-/-) mice. Further, LPS reduced the number of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra (SN) by 23% at 7-months post-treatment, which progressed to 47% at 10 months. Together, these data demonstrate that through TNFalpha, peripheral inflammation in adult animals can: (1) activate brain microglia to produce chronically elevated pro-inflammatory factors; (2) induce delayed and progressive loss of DA neurons in the SN. These findings provide valuable insight into the potential pathogenesis and self-propelling nature of Parkinson's disease. (c) 2007 Wiley-Liss, Inc.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Free radicals, antioxidants and functional foods: Impact on human health

            In recent years, there has been a great deal of attention toward the field of free radical chemistry. Free radicals reactive oxygen species and reactive nitrogen species are generated by our body by various endogenous systems, exposure to different physiochemical conditions or pathological states. A balance between free radicals and antioxidants is necessary for proper physiological function. If free radicals overwhelm the body's ability to regulate them, a condition known as oxidative stress ensues. Free radicals thus adversely alter lipids, proteins, and DNA and trigger a number of human diseases. Hence application of external source of antioxidants can assist in coping this oxidative stress. Synthetic antioxidants such as butylated hydroxytoluene and butylated hydroxyanisole have recently been reported to be dangerous for human health. Thus, the search for effective, nontoxic natural compounds with antioxidative activity has been intensified in recent years. The present review provides a brief overview on oxidative stress mediated cellular damages and role of dietary antioxidants as functional foods in the management of human diseases.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The stressed hippocampus, synaptic plasticity and lost memories.

              Stress is a biologically significant factor that, by altering brain cell properties, can disturb cognitive processes such as learning and memory, and consequently limit the quality of human life. Extensive rodent and human research has shown that the hippocampus is not only crucially involved in memory formation, but is also highly sensitive to stress. So, the study of stress-induced cognitive and neurobiological sequelae in animal models might provide valuable insight into the mnemonic mechanisms that are vulnerable to stress. Here, we provide an overview of the neurobiology of stress memory interactions, and present a neural endocrine model to explain how stress modifies hippocampal functioning.
                Bookmark

                Author and article information

                Journal
                Avicenna J Phytomed
                Avicenna J Phytomed
                IJP
                Avicenna Journal of Phytomedicine
                Mashhad University of Medical Sciences (Mashhad, Iran )
                2228-7930
                2228-7949
                Jan-Feb 2021
                : 11
                : 1
                : 79-90
                Affiliations
                [1] Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                Author notes
                [* ]Corresponding Author: Tel:+98-31-37929181, Fax:+98-31-36688597, rajaeiz@med.mui.ac.ir
                Article
                AJP-11-079
                10.22038/AJP.2020.16490
                7885005
                33628722
                4e20ebbd-6f7e-4c73-b0f1-744d887c0430

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 April 2020
                : 21 June 2020
                : 23 June 2020
                Categories
                Original Research Article

                crocin,lipopolysaccharide,memory,interleukin-1β,oxidative stress,systemic inflammation

                Comments

                Comment on this article