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      Sodium ozagrel and atorvastatin for type 2 diabetes patients with lacunar cerebral infarction

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          Abstract

          BACKGROUND

          The main pathological factor of cerebral infarction is atherosclerosis, which is the pathological process of chronic inflammatory diseases such as vascular smooth muscle hyperplasia, inflammatory cell infiltration, extracellular matrix increase, and thrombosis. At present, the focus of clinical treatment is anti-platelet aggregation and improving blood status, and current research is limited to improving symptoms only.

          AIM

          To observe the effect of sodium ozagrel and atorvastatin on type 2 diabetes patients with lacunar cerebral infarction.

          METHODS

          Eighty-two patients with type 2 diabetes and lacunar cerebral infarction admitted to our hospital from January 2018 to February 2020 were equally categorized into two groups according to their treatment method. The control group was administered atorvastatin, and the observation group was administered sodium ozagrel combined with atorvastatin. The National Institutes of Health stroke scale (NIHSS) score, activities of daily living (ADL) score, blood glucose, lipid levels, inflammatory factors, high-mobility group box 1 (HMGB1) levels, paraoxonase-1 (PON-1) levels, erythrocyte sedimentation rate (ESR), and macrophage migration inhibitory factor (MIF) levels were recorded before and after treatment. The total effective rate and adverse reaction rate of the two groups were analyzed.

          RESULTS

          The total effective rate of the observation group (94.00%) was significantly higher than that of the control group (80.00%) ( χ 2 = 3.998; P = 0.046). The blood glucose indexes, total cholesterol levels, triglyceride levels, low-density lipoprotein cholesterol levels, high-sensitivity C-reactive protein levels, interleukin-1β levels, tumor necrosis factor-α levels, HMGB1 Levels, ESR, MIF levels, platelet aggregation rates, and plasma viscosity of the two groups decreased after treatment; however, high-density lipoprotein cholesterol and PON-1 Levels increased after treatment. After treatment, the blood glucose indexes; blood lipid indexes; inflammatory factors; HMGB1, PON-1, and MIF levels; ESR; platelet aggregation rate; and plasma viscosity of the observation group were better than those of the control group ( P < 0.05). After treatment, all patients in the observation group had higher ADL scores and lower NIHSS scores than those in the control group ( P < 0.05).

          CONCLUSION

          Sodium ozagrel with atorvastatin can reduce inflammatory reactions; regulate ESR and HMGB1, PON-1, and MIF levels; control blood glucose and lipid indexes; and alleviate nerve injury without increasing adverse effects of atorvastatin alone.

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          Most cited references50

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          Type 2 Diabetes and its Impact on the Immune System

          Introduction: Type 2 Diabetes (T2D) is a major health problem worldwide. This metabolic disease is indicated by high blood glucose levels due to insufficient insulin production by the pancreas. An inflammatory response occurs as a result of the immune response to high blood glucose levels as well as the presence of inflammatory mediators produced by adipocytes and macrophages in fat tissue. This low and chronic inflammation damages the pancreatic beta cells and leads to insufficient insulin production, which results in hyperglycemia. Hyperglycemia in diabetes is thought to cause dysfunction of the immune response, which fails to control the spread of invading pathogens in diabetic subjects. Therefore, diabetic subjects are known to more susceptible to infections. The increased prevalence of T2D will increase the incidence of infectious diseases and related comorbidities. Objective: This review provides an overview of the immunological aspect of T2D and the possible mechanisms that result in increased infections in diabetics. Conclusion: A better understanding of how immune dysfunctions occur during hyperglycemia can lead to novel treatments and preventions for infectious diseases and T2D comorbidities, thus improving the outcome of infectious disease treatment in T2D patients.
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            Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes.

            The clinical correlations linking diabetes mellitus with accelerated atherosclerosis, cardiomyopathy, and increased post-myocardial infarction fatality rates are increasingly understood in mechanistic terms. The multiple mechanisms discussed in this review seem to share a common element: prolonged increases in reactive oxygen species (ROS) production in diabetic cardiovascular cells. Intracellular hyperglycemia causes excessive ROS production. This activates nuclear poly(ADP-ribose) polymerase, which inhibits GAPDH, shunting early glycolytic intermediates into pathogenic signaling pathways. ROS and poly(ADP-ribose) polymerase also reduce sirtuin, PGC-1α, and AMP-activated protein kinase activity. These changes cause decreased mitochondrial biogenesis, increased ROS production, and disturbed circadian clock synchronization of glucose and lipid metabolism. Excessive ROS production also facilitates nuclear transport of proatherogenic transcription factors, increases transcription of the neutrophil enzyme initiating NETosis, peptidylarginine deiminase 4, and activates the NOD-like receptor family, pyrin domain-containing 3 inflammasome. Insulin resistance causes excessive cardiomyocyte ROS production by increasing fatty acid flux and oxidation. This stimulates overexpression of the nuclear receptor PPARα and nuclear translocation of forkhead box O 1, which cause cardiomyopathy. ROS also shift the balance between mitochondrial fusion and fission in favor of increased fission, reducing the metabolic capacity and efficiency of the mitochondrial electron transport chain and ATP synthesis. Mitochondrial oxidative stress also plays a central role in angiotensin II-induced gap junction remodeling and arrhythmogenesis. ROS contribute to sudden death in diabetics after myocardial infarction by increasing post-translational protein modifications, which cause increased ryanodine receptor phosphorylation and downregulation of sarco-endoplasmic reticulum Ca(++)-ATPase transcription. Increased ROS also depress autonomic ganglion synaptic transmission by oxidizing the nAch receptor α3 subunit, potentially contributing to the increased risk of fatal cardiac arrhythmias associated with diabetic cardiac autonomic neuropathy.
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              Differentiation of Diabetes by Pathophysiology, Natural History, and Prognosis

              The American Diabetes Association, JDRF, the European Association for the Study of Diabetes, and the American Association of Clinical Endocrinologists convened a research symposium, “The Differentiation of Diabetes by Pathophysiology, Natural History and Prognosis” on 10–12 October 2015. International experts in genetics, immunology, metabolism, endocrinology, and systems biology discussed genetic and environmental determinants of type 1 and type 2 diabetes risk and progression, as well as complications. The participants debated how to determine appropriate therapeutic approaches based on disease pathophysiology and stage and defined remaining research gaps hindering a personalized medical approach for diabetes to drive the field to address these gaps. The authors recommend a structure for data stratification to define the phenotypes and genotypes of subtypes of diabetes that will facilitate individualized treatment.
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                Author and article information

                Contributors
                Journal
                World J Diabetes
                WJD
                World Journal of Diabetes
                Baishideng Publishing Group Inc
                1948-9358
                15 December 2021
                15 December 2021
                : 12
                : 12
                : 2096-2106
                Affiliations
                Department of Pharmacy, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China
                Department of Pharmacy, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China
                Department of Pharmacy, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China
                Department of Pharmacy, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China
                Department of Pharmacy, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China. mhy2021888@ 123456163.com
                Author notes

                Author contributions: Yu Y and Ma HY designed the research study; Wang L and Yu Y performed the research; Zhu X, Liu YF and Ma HY analyzed the data and wrote the manuscript; and all authors have read and approve the final manuscript.

                Corresponding author: Hai-Ying Ma, MHSc, Chief Pharmacist, Department of Pharmacy, The Fourth Affiliated Hospital of China Medical University, No. 4 Chongshan Road, Huanggu District, Shenyang 110032, Liaoning Province, China. mhy2021888@ 123456163.com

                Article
                jWJD.v12.i12.pg2096
                10.4239/wjd.v12.i12.2096
                8696649
                51cb7926-4a0d-4410-af9a-61e53608e20c
                ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.

                This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

                History
                : 2 September 2021
                : 15 October 2021
                : 10 December 2021
                Categories
                Retrospective Study

                sodium ozagrel,atorvastatin,type 2 diabetes,lacunar infarction,inflammatory response,nerve damage

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