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      Gastroprotective effects of Polygonatum odoratum in rodents by regulation of apoptotic proteins and inflammatory cytokines

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          Abstract

          In an increasing interest in natural antiulcer compounds that may have gastric healing effects and possibly prevent ulcer recurrence, Polygonatum odoratum appears as a strong candidate. The gastroprotective potentials of P. odoratum rhizome extract (PORE) were explored on ethanol-induced gastric ulceration in rats. Sprague Dawley rats were caged in 5 groups, normal and ulcer control rats received CMC (1% carboxymethyl cellulose). Omeprazole (20 mg/kg) was given to reference Rats. Experimental rats were treated with 250 mg/kg and 500 mg/kg PORE, respectively. After an hour, the normal control rats received 1% CMC, whereas rat groups 2–5 were given absolute ethanol by oral gavage. After 60 min, rats received anesthesia and were sacrificed. Dissected gastric tissue was analyzed by histopathological and immunohistochemical techniques. PORE treatment significantly lowered the ethanol-induced gastric injury, as shown by up-surging gastric pH and mucus content, reduced leukocyte infiltration, lower ulcerative areas in mucosal layers, and increased antioxidants (SOD and CAT) and (MDA) levels. Furthermore, PORE pre-treated rats showed significantly increased expression of the Periodic acid-Schiff (PAS), HSP-70 protein, and decreased Bax protein in their gastric epithelial layers. PORE treatment showed an important regulation of inflammatory cytokines shown by decreasing the TNF-a, and IL-6 and increasing the IL-10 values. The detected biological activity of PORE is encouraging and presents the scientific evidence for its traditional use as a gastroprotection agent however further studies are required to determine the exact phytochemicals and mechanism pathway responsible for this bioactivity.

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          Most cited references65

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          Mortality due to low-quality health systems in the universal health coverage era: a systematic analysis of amenable deaths in 137 countries

          Summary Background Universal health coverage has been proposed as a strategy to improve health in low-income and middle-income countries (LMICs). However, this is contingent on the provision of good-quality health care. We estimate the excess mortality for conditions targeted in the Sustainable Development Goals (SDG) that are amenable to health care and the portion of this excess mortality due to poor-quality care in 137 LMICs, in which excess mortality refers to deaths that could have been averted in settings with strong health systems. Methods Using data from the 2016 Global Burden of Disease study, we calculated mortality amenable to personal health care for 61 SDG conditions by comparing case fatality between each LMIC with corresponding numbers from 23 high-income reference countries with strong health systems. We used data on health-care utilisation from population surveys to separately estimate the portion of amenable mortality attributable to non-utilisation of health care versus that attributable to receipt of poor-quality care. Findings 15·6 million excess deaths from 61 conditions occurred in LMICs in 2016. After excluding deaths that could be prevented through public health measures, 8·6 million excess deaths were amenable to health care of which 5·0 million were estimated to be due to receipt of poor-quality care and 3·6 million were due to non-utilisation of health care. Poor quality of health care was a major driver of excess mortality across conditions, from cardiovascular disease and injuries to neonatal and communicable disorders. Interpretation Universal health coverage for SDG conditions could avert 8·6 million deaths per year but only if expansion of service coverage is accompanied by investments into high-quality health systems. Funding Bill & Melinda Gates Foundation.
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            Nrf2-Keap1 defines a physiologically important stress response mechanism.

            The transcription factor Nrf2 regulates the basal and inducible expression of numerous detoxifying and antioxidant genes. The cytoplasmic protein Keap1 interacts with Nrf2 and represses its function. Analysis of keap1-knockout mice provides solid evidence that Keap1 acts as a negative regulator of Nrf2 and as a sensor of xenobiotic and oxidative stresses. The simultaneous ablation of the keap1 and nrf2 genes reversed all apparent phenotypes of the Keap1-deficient mice, suggesting that Nrf2 is a primary target of Keap1. The Nrf2-Keap1 system is now recognized as one of the major cellular defence mechanisms against oxidative and xenobiotic stresses. Furthermore, extensive studies have suggested that the Nrf2-Keap1 system contributes to protection against various pathologies, including carcinogenesis, liver toxicity, respiratory distress and inflammation.
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              Long-term proton pump inhibitors and risk of gastric cancer development after treatment for Helicobacter pylori: a population-based study

              Objective Proton pump inhibitors (PPIs) is associated with worsening of gastric atrophy, particularly in Helicobacter pylori (HP)-infected subjects. We determined the association between PPIs use and gastric cancer (GC) among HP-infected subjects who had received HP therapy. Designs This study was based on a territory-wide health database of Hong Kong. We identified adults who had received an outpatient prescription of clarithromycin-based triple therapy between year 2003 and 2012. Patients who failed this regimen, and those diagnosed to have GC within 12 months after HP therapy, or gastric ulcer after therapy were excluded. Prescriptions of PPIs or histamine-2 receptor antagonists (H2RA) started within 6 months before GC were excluded to avoid protopathic bias. We evaluated GC risk with PPIs by Cox proportional hazards model with propensity score adjustment. H2RA was used as a negative control exposure. Result Among the 63 397 eligible subjects, 153 (0.24%) developed GC during a median follow-up of 7.6 years. PPIs use was associated with an increased GC risk (HR 2.44, 95% CI 1.42 to 4.20), while H2RA was not (HR 0.72, 95% CI 0.48 to 1.07). The risk increased with duration of PPIs use (HR 5.04, 95% CI 1.23 to 20.61; 6.65, 95% CI 1.62 to 27.26 and 8.34, 95% CI 2.02 to 34.41 for ≥1 year, ≥2 years and ≥3 years, respectively). The adjusted absolute risk difference for PPIs versus non-PPIs use was 4.29 excess GC (95% CI 1.25 to 9.54) per 10 000 person-years. Conclusion Long-term use of PPIs was still associated with an increased GC risk in subjects even after HP eradication therapy.
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                Author and article information

                Contributors
                Journal
                Saudi J Biol Sci
                Saudi J Biol Sci
                Saudi Journal of Biological Sciences
                Elsevier
                1319-562X
                2213-7106
                08 May 2023
                June 2023
                08 May 2023
                : 30
                : 6
                : 103678
                Affiliations
                [a ]College of Science and Arts, Alkamil Branch, University of Jeddah, Alkamil 21931, Saudi Arabia
                [b ]Indigenous Knowledge and Heritage Centre, Ghibaish College of Science and Technology, 110 Ghibaish, Sudan
                [c ]Department of Medical Laboratory Technology, Erbil Technical Health and Medical College, Erbil Polytechnic University, Erbil 44001, Iraq
                [d ]Department of Biological Sciences, Faculty of Science, University of Jeddah, Jeddah, Saudi Arabia
                [e ]Central Public Health Laboratories, Ministry of Health, Muscat 111, Oman
                [f ]Department of Medical Microbiology, College of Science, Cihan University-Erbil, Erbil 44001, Kurdistan Region, Iraq
                Author notes
                [* ]Corresponding author. ahmed.abuljabbar@ 123456epu.edu.iq
                Article
                S1319-562X(23)00123-7 103678
                10.1016/j.sjbs.2023.103678
                10230262
                37266408
                82310354-c72c-49f7-878f-8e44797e8a3e
                © 2023 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 22 February 2023
                : 11 April 2023
                : 27 April 2023
                Categories
                Original Article

                polygonatum odoratum rhizome extract,oxidative stress,stomach ulcer,histology,immunohistochemistry,acute toxicity

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