{"title":"Screening of anti-Parkinson activity of tannic acid via antioxidant and neuroprotection in Wistar rats","authors":"Himani Badoni , Sakshi Painuli , Sachin Panwar , Promila Sharma , Prabhakar Semwal","doi":"10.1016/j.dscb.2023.100109","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Inflammation in the brain is a severe pathological state to facilitate neurodegenerative disorders. Various inflammatory mediators, such as tumor necrosis factor-α (TNF-α), nitric oxide (NO), interleukin-1 (IL-1), and prostaglandins, promote inflammation. The expression of these major inflammatory mediators is induced by the activation of microglia and astrocytes. Diseases likewise Parkinson's disease (PD), Alzheimer's disease (AD) and multiple sclerosis are caused by uncontrolled release of pro-inflammatory cytokines.</p></div><div><h3>Methods</h3><p>Acute (5, 50, and 300 mg kg<sup>−1</sup>), subacute study (30, 100, and 300 mg kg<sup>−1</sup>) toxicity in rats. In addition, consequence of tannic acid (TA) on haloperidol stimulated catalepsy model of PD in Wistar rats (6–8 weeks) was analysed. Toxicity study of TA has been done to identify the safer dose for experimental animals.</p></div><div><h3>Results</h3><p><em>In vivo</em> antioxidant assays demonstrate the suppressed amount of oxidative stress caused due to lipid peroxidation (LPO) and elevated amount of reduced glutathione (GSH),superoxide dismutase (SOD) and catalase (CAT) after assessment with TA as compared to those in only haloperidol treated rats. TNF-α and NO amount were too found to be reduced in rat model of PD when pretreated with TA. haematological analyses also demonstrated the normal level of haemoglobin (Hb), Red blood cell (RBC) count, White blood cell(WBC) count, lymphocyte count, granulocyte count, mean corpuscular volume (MCV) and platelet count in rats pretreated with TA. Histopathological analysis of rat brain tissue showed neuroprotection in groups pretreated with TA. In addition, ADMET results based on structure to activity calculation related to pharmacokinetics and toxicity assessment revealed that TA had reasonably acceptable qualities. These attributes add to our understanding of structural aspects that may boost the bioavailability of TA before going on to the early stages of medication development.</p></div><div><h3>Conclusion</h3><p>Results obtained from the present study suggest that TA have potential to be extended as effective curative candidate for PD and various neurodegenerative diseases.</p></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"13 ","pages":"Article 100109"},"PeriodicalIF":0.0000,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266645932300046X/pdfft?md5=8b58f06ddeb928ac3c47062aae39d4ef&pid=1-s2.0-S266645932300046X-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain disorders (Amsterdam, Netherlands)","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S266645932300046X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Background
Inflammation in the brain is a severe pathological state to facilitate neurodegenerative disorders. Various inflammatory mediators, such as tumor necrosis factor-α (TNF-α), nitric oxide (NO), interleukin-1 (IL-1), and prostaglandins, promote inflammation. The expression of these major inflammatory mediators is induced by the activation of microglia and astrocytes. Diseases likewise Parkinson's disease (PD), Alzheimer's disease (AD) and multiple sclerosis are caused by uncontrolled release of pro-inflammatory cytokines.
Methods
Acute (5, 50, and 300 mg kg−1), subacute study (30, 100, and 300 mg kg−1) toxicity in rats. In addition, consequence of tannic acid (TA) on haloperidol stimulated catalepsy model of PD in Wistar rats (6–8 weeks) was analysed. Toxicity study of TA has been done to identify the safer dose for experimental animals.
Results
In vivo antioxidant assays demonstrate the suppressed amount of oxidative stress caused due to lipid peroxidation (LPO) and elevated amount of reduced glutathione (GSH),superoxide dismutase (SOD) and catalase (CAT) after assessment with TA as compared to those in only haloperidol treated rats. TNF-α and NO amount were too found to be reduced in rat model of PD when pretreated with TA. haematological analyses also demonstrated the normal level of haemoglobin (Hb), Red blood cell (RBC) count, White blood cell(WBC) count, lymphocyte count, granulocyte count, mean corpuscular volume (MCV) and platelet count in rats pretreated with TA. Histopathological analysis of rat brain tissue showed neuroprotection in groups pretreated with TA. In addition, ADMET results based on structure to activity calculation related to pharmacokinetics and toxicity assessment revealed that TA had reasonably acceptable qualities. These attributes add to our understanding of structural aspects that may boost the bioavailability of TA before going on to the early stages of medication development.
Conclusion
Results obtained from the present study suggest that TA have potential to be extended as effective curative candidate for PD and various neurodegenerative diseases.
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