Syringic acid (SA) is a naturally occurring O-methylated trihydroxybenzoic acid present in wine and released as a breakdown product of malvidin, a primary plant pigment (an anthocyanidin). In this study, the neuroprotective efficacy of syringic acid (SA) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probencid (MPTP/p) induced mouse model of PD was investigated. The C57BL/6 mice were given 10 doses of MPTP/p for five consecutive weeks with 3.5day interval. Administration of MPTP/p led to reduced motor coordination, neurochemicals and tyrosine hydroxylase (TH), dopamine transporter (DAT) and vesicular monoamine transporter-2 (VMAT2) expression. In addition, increased oxidative stress markers and the expression of inflammatory markers, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2). Pre-oral treatment with SA (20mg/kg) was found to improve the MPTP/p-induced impaired motor functions by restoring the catecholamine content and antioxidant enzymes level. In addition, it ameliorated the expressions of TH, DAT and VMAT2 and also significantly attenuated MPTP/p-induced increased inflammatory markers expressions. These results partially explain the pharmacological efficacy of SA as a potential therapeutic agent for the treatment of MPTP/p-induced mice model of PD, together with its neuroprotective effect and reduce the progression of PD.
{"title":"Effects of syringic acid on chronic MPTP/probenecid induced motor dysfunction, dopaminergic markers expression and neuroinflammation in C57BL/6 mice","authors":"Karamkolly Raghavan Rekha , Govindasamy Pushpavathi Selvakumar , Ramu Inmozhi Sivakamasundari","doi":"10.1016/j.biomag.2014.02.004","DOIUrl":"10.1016/j.biomag.2014.02.004","url":null,"abstract":"<div><p><span>Syringic acid (SA) is a naturally occurring </span><em>O</em><span>-methylated trihydroxybenzoic acid present in wine and released as a breakdown product of malvidin<span><span>, a primary plant pigment (an anthocyanidin). In this study, the neuroprotective efficacy of syringic acid (SA) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probencid (MPTP/p) induced mouse model of </span>PD was investigated. The C57BL/6 mice were given 10 doses of MPTP/p for five consecutive weeks with 3.5</span></span> <span><span><span>day interval. Administration of MPTP/p led to reduced motor coordination, neurochemicals and tyrosine hydroxylase (TH), </span>dopamine transporter (DAT) and vesicular monoamine transporter-2 (VMAT2) expression. In addition, increased </span>oxidative stress<span> markers and the expression of inflammatory markers, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2). Pre-oral treatment with SA (20</span></span> <span>mg/kg) was found to improve the MPTP/p-induced impaired motor functions by restoring the catecholamine<span> content and antioxidant enzymes level. In addition, it ameliorated the expressions of TH, DAT and VMAT2 and also significantly attenuated MPTP/p-induced increased inflammatory markers expressions. These results partially explain the pharmacological efficacy of SA as a potential therapeutic agent for the treatment of MPTP/p-induced mice model of PD, together with its neuroprotective effect and reduce the progression of PD.</span></span></p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 95-104"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.02.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74155437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2013.12.002
Manigandan Krishnan, Richard L. Jayaraj, Jayasekar Megala, Namasivayam Elangovan
Purpose
Ulcerative colitis (UC) is associated with tainted neutrophil infiltration, deregulated pro-inflammatory mediators, characterized by severe oxidative stress of the intestine. In the present study, an effort was made to evaluate the effect of methanolic fractions of Eupatorium triplinerve (E.triplinerve) (ET) on acetic acid induced ulcerative colitis in male adult mice.
Methods
Colitis in mice was induced with 3.0% acetic acid (v/v) in saline via rectal route. Pre-intervention with E.triplinerve extract (100 mg and 200 mg kg−1 body weight, oral) and reference drug ranitidine (50 mg kg−1 body weight used as reference, oral) 4 days before induction of colitis and was extended up to 8 days.
Results
The phase of inflammation before E.triplinerve extract pre-treatment significantly showed attenuated macroscopic damage, argyrophilic nuclear organization regions (AgNORs) count and histological changes. Similarly, extract also effectively detracts the activity of both Myeloperoxidase (MPO) and Malondialdehyde (MDA) levels by enhancing the cellular antioxidant enzyme levels (Glutathione-s-transferase [GST], Glutathione peroxidise [GPx] and Catalase [CAT]) at the site of ulceration.
Conclusions
The E.triplinerve based therapy resolved that some constituents in extract have an antiulcer effect against UC at colon specific area through its inviolable radical scavenging activity.
目的溃疡性结肠炎(UC)与中性粒细胞浸润污染、促炎介质失调有关，其特征是肠道严重氧化应激。本研究探讨了紫茎泽兰(E. triplinerve) (ET)甲醇组分对醋酸诱导的成年雄性小鼠溃疡性结肠炎的影响。方法用3.0%醋酸(v/v)灌胃盐水经直肠诱导小鼠结肠炎。在结肠炎诱导前4天给予三叶麻提取物(100 mg和200 mg kg - 1体重，口服)和参比药物雷尼替丁(50 mg kg - 1体重，口服)进行干预，并延长至8天。结果三叶麻提取物预处理前炎症期宏观损伤、亲银核组织区(AgNORs)计数及组织学改变明显减轻。同样，提取物还通过提高溃疡部位的细胞抗氧化酶(谷胱甘肽-s转移酶[GST]、谷胱甘肽过氧化物酶[GPx]和过氧化氢酶[CAT])水平，有效降低髓过氧化物酶(MPO)和丙二醛(MDA)水平的活性。结论三叶藤提取物中部分成分通过其不可侵犯的自由基清除活性，在结肠特定区域对UC具有抗溃疡作用。
{"title":"Antioxidant mediated antiulcer effect of Eupatorium triplinerve Vahl against acetic acid induced ulcerative colitis in mice","authors":"Manigandan Krishnan, Richard L. Jayaraj, Jayasekar Megala, Namasivayam Elangovan","doi":"10.1016/j.biomag.2013.12.002","DOIUrl":"10.1016/j.biomag.2013.12.002","url":null,"abstract":"<div><h3>Purpose</h3><p><span>Ulcerative colitis<span> (UC) is associated with tainted neutrophil infiltration<span>, deregulated pro-inflammatory mediators, characterized by severe oxidative stress of the intestine. In the present study, an effort was made to evaluate the effect of methanolic fractions of </span></span></span><span><em>Eupatorium</em><em> triplinerve</em></span> (<em>E.</em> <em>triplinerve</em>) (ET) on acetic acid induced ulcerative colitis in male adult mice.</p></div><div><h3>Methods</h3><p><span>Colitis in mice was induced with 3.0% acetic acid (v/v) in saline via rectal route. Pre-intervention with </span><em>E.</em> <em>triplinerve</em> extract (100<!--> <!-->mg and 200<!--> <!-->mg<!--> <!-->kg<sup>−1</sup><span> body weight, oral) and reference drug<span> ranitidine (50</span></span> <!-->mg<!--> <!-->kg<sup>−1</sup> body weight used as reference, oral) 4<!--> <!-->days before induction of colitis and was extended up to 8<!--> <!-->days.</p></div><div><h3>Results</h3><p>The phase of inflammation before <em>E.</em> <em>triplinerve</em><span><span> extract pre-treatment significantly showed attenuated macroscopic damage, argyrophilic nuclear organization regions (AgNORs) count and histological changes. Similarly, extract also effectively detracts the activity of both Myeloperoxidase (MPO) and </span>Malondialdehyde<span><span> (MDA) levels by enhancing the cellular antioxidant enzyme levels (Glutathione-s-transferase [GST], </span>Glutathione<span><span> peroxidise [GPx] and Catalase [CAT]) at the site of </span>ulceration.</span></span></span></p></div><div><h3>Conclusions</h3><p>The <em>E.</em> <em>triplinerve</em><span> based therapy resolved that some constituents in extract have an antiulcer effect against UC at colon specific area through its inviolable radical scavenging activity.</span></p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 153-160"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2013.12.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84683715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2014.01.001
Ezar Hafez, Ehab Tousson
The heart is a major target organ for thyroid hormone action and marked changes occur in cardiac function in the case of hypo- or hyperthyroidism. Hyperthyroidism is a common metabolic disorder with prominent cardiovascular manifestation. We studied the changes in the heart structure and functions of hyperthyroid rat and ameliorating and protective role of ascorbic acid in treatment. Fourty male albino rats were equally divided into five groups; the first and second groups were the control and ascorbic acid groups respectively. Third group was the hyperthyroid rat group while 4th and 5th groups were co- and post-treated hyperthyroid rat with ascorbic acid respectively. Serum T3 and T4 levels were significantly increased also; TSH levels were significantly decreased in hyperthyroid rat as compared to control rat groups. Cholesterol, triglyceride, LDL-c and VLDL-c were significantly decreased when compared with control group. Many of abnormalities as severe hydrophobic changes of myofibrillar structure with striations, hypertrophy, cytoplasmic vacuoles and marked increase in desmin immunoreactivity were observed in left ventricle in hyperthyroid rats. Treatment with ascorbic acid helps in improving the adverse effect of hypothyroidism and also the histopathological and desmin immunoreactivity results confirms this finding.
{"title":"Thyroxine-induced cardiac hypertrophy: Role of ascorbic acid in treatment","authors":"Ezar Hafez, Ehab Tousson","doi":"10.1016/j.biomag.2014.01.001","DOIUrl":"10.1016/j.biomag.2014.01.001","url":null,"abstract":"<div><p><span><span><span>The heart is a major target organ for thyroid hormone action and marked changes occur in cardiac function in the case of hypo- or hyperthyroidism. Hyperthyroidism is a common </span>metabolic disorder with prominent cardiovascular manifestation. We studied the changes in the heart structure and functions of hyperthyroid rat and ameliorating and protective role of </span>ascorbic acid<span> in treatment<span>. Fourty male albino rats were equally divided into five groups; the first and second groups were the control and ascorbic acid groups respectively. Third group was the hyperthyroid rat group while 4</span></span></span><sup>th</sup> and 5<sup>th</sup> groups were co- and post-treated hyperthyroid rat with ascorbic acid respectively. Serum T<sub>3</sub> and T<sub>4</sub><span><span><span> levels were significantly increased also; TSH levels were significantly decreased in hyperthyroid rat as compared to control rat groups. Cholesterol, triglyceride<span>, LDL-c and VLDL-c were significantly decreased when compared with control group. Many of abnormalities as severe hydrophobic changes of myofibrillar structure with striations, hypertrophy, cytoplasmic vacuoles and marked increase in </span></span>desmin </span>immunoreactivity<span> were observed in left ventricle in hyperthyroid rats. Treatment with ascorbic acid helps in improving the adverse effect of hypothyroidism and also the histopathological and desmin immunoreactivity results confirms this finding.</span></span></p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 161-167"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.01.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78065777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2014.01.004
Abdel-Tawab H. Mossa , Tarek M. Heikal , Enayat Abdel Aziz Omara
Purpose
The widespread use of organophosphorus insecticides (OPIs) consequently leads to the exposure of manufacturing workers, field applicators, the ecosystem, and finally the public to the possible toxic effects of OPIs. In addition, drugs or pharmaceutical products, which are used to cure diseases, are also xenobiotics with both therapeutic/toxic potentials. It is evident from the literature, which is very limited, that drug/insecticide interactions can result in altered response/toxicity, which is of clinical relevance. The aim of the present study was designed to assess the adverse effects of exposure to aspirin and diazinon and their combination on liver of male rats and hepatoprotective potential of selenium (Se).
Methods
Rats were oral administered with vehicle, acetyl salicylic acid (ASA) at the maximum administration dose (1350 mg/personal/day = 22.5 mg/kg. b.wt.), diazinon (DIA) at 20 mg/kg. b.wt. and Se at a dose of 200 μg/kg b.wt./day and their combinations for 28 consecutive days. Serum liver biomarkers, e.g. ALT&AST, ALP, ChE, LDH, albumin, total protein were determined as well as histological and histochemical studies.
Results
Body weight was statistically (P ≤ 0.05) decreased, while relative liver weight was statistically (P ≤ 0.05) increased in DIA and ASA + DIA-treated groups. The activities of serum aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were statistically (P ≤ 0.05) increased, while the activity of cholinesterase (ChE) was decreased in rats exposed to DIA, ASA and DIA + ASA. In addition, administration of DIA, ASA and their combination resulted in damage of liver structures and increase in the immunoreactivity of caspase-3 expression in the cytoplasm of the hepatocytes as compared to the control group. Combination therapy with Se significantly (P ≤ 0.05) restored these alterations to within the normal limits and prevents disruptions of liver structures.
Conclusions
The present study indicates that liver enzymes, histopathology and immunoreactivity of caspase-3 would trigger ASA- and DIA-induced liver injury. The severities of such observations were more pronounced in their combined exposure. Combination therapy with Se restored these alterations to within the normal limits and prevents disruptions of liver structures. The data throw light on the problem of simultaneous exposure to OPIs and commonly used drugs especially that are metabolised by CYP450. Accordingly, ASA should be avoided since many of the adverse effects associated with these d
{"title":"Liver damage associated with exposure to aspirin and diazinon in male rats and the ameliorative effect of selenium","authors":"Abdel-Tawab H. Mossa , Tarek M. Heikal , Enayat Abdel Aziz Omara","doi":"10.1016/j.biomag.2014.01.004","DOIUrl":"10.1016/j.biomag.2014.01.004","url":null,"abstract":"<div><h3>Purpose</h3><p><span><span>The widespread use of organophosphorus insecticides (OPIs) consequently leads to the exposure of manufacturing workers, field applicators, the ecosystem, and finally the public to the possible toxic effects of OPIs. In addition, </span>drugs or pharmaceutical products, which are used to cure diseases, are also </span>xenobiotics<span> with both therapeutic/toxic potentials. It is evident from the literature, which is very limited, that drug/insecticide interactions can result in altered response/toxicity, which is of clinical relevance. The aim of the present study was designed to assess the adverse effects of exposure to aspirin<span> and diazinon and their combination on liver of male rats and hepatoprotective potential of selenium (Se).</span></span></p></div><div><h3>Methods</h3><p>Rats were oral administered with vehicle, acetyl salicylic acid (ASA) at the maximum administration dose (1350<!--> <!-->mg/personal/day<!--> <!-->=<!--> <!-->22.5<!--> <!-->mg/kg. b.wt.), diazinon (DIA) at 20<!--> <!-->mg/kg. b.wt. and Se at a dose of 200<!--> <span><span>μg/kg b.wt./day and their combinations for 28 consecutive days. Serum liver biomarkers, e.g. ALT&AST, ALP<span>, ChE, </span></span>LDH, albumin, total protein were determined as well as histological and histochemical studies.</span></p></div><div><h3>Results</h3><p>Body weight was statistically (<em>P</em> <!-->≤<!--> <!-->0.05) decreased, while relative liver weight was statistically (<em>P</em> <!-->≤<!--> <!-->0.05) increased in DIA and ASA<!--> <!-->+<!--> <!-->DIA-treated groups. The activities of serum aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were statistically (<em>P</em> <!-->≤<!--> <!-->0.05) increased, while the activity of cholinesterase (ChE) was decreased in rats exposed to DIA, ASA and DIA<!--> <!-->+<!--> <span>ASA. In addition, administration of DIA, ASA and their combination resulted in damage of liver structures and increase in the immunoreactivity of caspase-3 expression in the cytoplasm of the hepatocytes as compared to the control group. Combination therapy with Se significantly (</span><em>P</em> <!-->≤<!--> <!-->0.05) restored these alterations to within the normal limits and prevents disruptions of liver structures.</p></div><div><h3>Conclusions</h3><p><span>The present study indicates that liver enzymes, </span>histopathology<span> and immunoreactivity of caspase-3 would trigger ASA- and DIA-induced liver injury. The severities of such observations were more pronounced in their combined exposure. Combination therapy with Se restored these alterations to within the normal limits and prevents disruptions of liver structures. The data throw light on the problem of simultaneous exposure to OPIs and commonly used drugs especially that are metabolised by CYP450<span>. Accordingly, ASA should be avoided since many of the adverse effects associated with these d","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 137-145"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.01.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86561880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2014.01.005
A.R. Chopade, F.J. Sayyad
Objective
To evaluate the effects of Phyllanthus extracts on mechanical hyperalgesia induced by repeated intramuscular injections of acidic saline.
Materials and methods
The standardized aqueous extract of Phyllanthus amarus whole plant (PAAE), Standardized methanolic extract of P. amarus leaf (PAEE), the standardized hydro-methanolic extract of P. amarus leaf (PAHEE) and standardized hydroethanolic extract of P. fraternus whole plant (PFHEE) were tested in the fibromyalgic model of acid-induced chronic pain in the rats. Mechanical hyperalgesia was assessed by measuring the withdrawal thresholds to mechanical stimuli both to the ipsilateral as well as to the contralateral paws. On 22nd day, the animals were sacrificed and the gastrocnemius muscle at the site of injection was dissected for histopathological studies.
Results
PAAE, PAEE, PAHEE and PFHEE increased the mechanical withdrawal threshold (mechanical hyperalgesia) back towards the baseline responses. The percentage of maximum possible effectiveness and percentage inhibition of hyperalgesia also revealed the efficacy of Phyllanthus extracts. The multidose strategy did not cause tolerance.
Conclusion
The results of the present study suggest that in the present model, muscle-mediated pain can be alleviated by standardized extracts of Phyllanthus species and suggest that these can be useful in treatment of chronic musculoskeletal pain syndromes such as fibromyalgia.
{"title":"Antifibromyalgic activity of standardized extracts of Phyllanthus amarus and Phyllanthus fraternus in acidic saline induced chronic muscle pain","authors":"A.R. Chopade, F.J. Sayyad","doi":"10.1016/j.biomag.2014.01.005","DOIUrl":"10.1016/j.biomag.2014.01.005","url":null,"abstract":"<div><h3>Objective</h3><p>To evaluate the effects of <span><em>Phyllanthus</em></span><span> extracts on mechanical hyperalgesia<span> induced by repeated intramuscular injections of acidic saline.</span></span></p></div><div><h3>Materials and methods</h3><p>The standardized aqueous extract of <span><em>Phyllanthus amarus</em></span> whole plant (PAAE), Standardized methanolic extract of <em>P. amarus</em> leaf (PAEE), the standardized hydro-methanolic extract of <em>P. amarus</em> leaf (PAHEE) and standardized hydroethanolic extract of <em>P. fraternus</em><span><span> whole plant (PFHEE) were tested in the fibromyalgic model of acid-induced chronic pain in the rats. Mechanical hyperalgesia was assessed by measuring the withdrawal thresholds to mechanical stimuli both to the ipsilateral as well as to the contralateral paws. On 22nd day, the animals were sacrificed and the </span>gastrocnemius muscle at the site of injection was dissected for histopathological studies.</span></p></div><div><h3>Results</h3><p>PAAE, PAEE, PAHEE and PFHEE increased the mechanical withdrawal threshold (mechanical hyperalgesia) back towards the baseline responses. The percentage of maximum possible effectiveness and percentage inhibition of hyperalgesia also revealed the efficacy of <em>Phyllanthus</em> extracts. The multidose strategy did not cause tolerance.</p></div><div><h3>Conclusion</h3><p>The results of the present study suggest that in the present model, muscle-mediated pain can be alleviated by standardized extracts of <em>Phyllanthus</em><span><span> species and suggest that these can be useful in treatment of chronic </span>musculoskeletal pain<span> syndromes such as fibromyalgia.</span></span></p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 123-130"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.01.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82710138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2014.03.006
Huynh Thien Duc
Time passing drives all living organismes to cellular decline with age-associated dysfuntion, diseases and death. It appeared now that ageing like any biological process is surceptible to regulation. Environmental factors such as stimuli/stresses as well as endogenous factors, i.e., expression and mutation of some particular genes might act as the main regulators. Psychological factors as a human specific dimension could contribute in delaying the senescence decline.
{"title":"The biological time calendar","authors":"Huynh Thien Duc","doi":"10.1016/j.biomag.2014.03.006","DOIUrl":"10.1016/j.biomag.2014.03.006","url":null,"abstract":"<div><p>Time passing drives all living organismes to cellular decline with age-associated dysfuntion, diseases and death. It appeared now that ageing like any biological process<span> is surceptible to regulation. Environmental factors such as stimuli/stresses as well as endogenous factors, i.e., expression and mutation of some particular genes might act as the main regulators. Psychological factors as a human specific dimension could contribute in delaying the senescence decline.</span></p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 77-89"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.03.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80710219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Considering the importance of plant derived compounds in prevention of cellular damage caused by reactive oxygen species which has been implicated to several diseases, this present study was undertaken to evaluate the anticancer effects of coumarin by MTT assay, lipid peroxidation markers and antioxidants status against Hep2 cancer cells. A Hep2 cells was treated with different concentrations of coumarin (2.5–1000 μg/ml) for 24 h and its cytotoxicity effect were measured by MTT assay. Apoptosis was investigated in terms of acridine orange/ethidium bromide dual staining method and DNA fragmentation. Our present investigation showed that coumarin decreased cell viability with an IC50 value of 62.5 μg/ml. The IC50 was determined by dose response curve by plotting the graph of concentration versus % cell viability. Hep2 cancer cells showed decreased levels of lipid peroxidation with increased activities of enzymatic antioxidants. Among the various doses of coumarin (125, 250 and 500 μg/ml), 500 μg/ml dose significantly decreased lipid peroxidation and increased antioxidant activities. Moreover, coumarin inhibited Hep2 cell growth and showed typical characteristics of apoptosis including the morphological changes and DNA fragmentation. On the basis of these findings, coumarin may be considered as potential therapeutic intervention of human Hep2 cancer cells.
{"title":"Antiproliferative effect of coumarin by modulating oxidant/antioxidant status and inducing apoptosis in Hep2 cells","authors":"Sankaran Mirunalini, Krishnamoorthy Deepalakshmi, Jalagopal Manimozhi","doi":"10.1016/j.biomag.2014.01.006","DOIUrl":"10.1016/j.biomag.2014.01.006","url":null,"abstract":"<div><p><span><span>Considering the importance of plant derived compounds<span> in prevention of cellular damage caused by reactive oxygen species which has been implicated to several diseases, this present study was undertaken to evaluate the anticancer effects of </span></span>coumarin<span><span> by MTT assay<span>, lipid peroxidation markers and antioxidants status against Hep2 </span></span>cancer cells. A Hep2 cells was treated with different concentrations of coumarin (2.5–1000</span></span> <!-->μg/ml) for 24<!--> <span><span>h and its cytotoxicity effect were measured by MTT assay. Apoptosis was investigated in terms of acridine orange/ethidium bromide dual staining method and </span>DNA fragmentation<span>. Our present investigation showed that coumarin decreased cell viability with an IC</span></span><sub>50</sub> value of 62.5<!--> <!-->μg/ml. The IC<sub>50</sub> was determined by dose response curve by plotting the graph of concentration versus % cell viability. Hep2 cancer cells showed decreased levels of lipid peroxidation with increased activities of enzymatic antioxidants. Among the various doses of coumarin (125, 250 and 500<!--> <!-->μg/ml), 500<!--> <span>μg/ml dose significantly decreased lipid peroxidation and increased antioxidant activities. Moreover, coumarin inhibited Hep2 cell growth and showed typical characteristics of apoptosis including the morphological changes and DNA fragmentation. On the basis of these findings, coumarin may be considered as potential therapeutic intervention of human Hep2 cancer cells.</span></p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 131-135"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.01.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89548203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2014.01.002
Richard L. Jayaraj, Namasivayam Elangovan
Parkinson disease is a progressive neurodegenerative disorder characterized by the presence of Lewy bodies with dense α-synuclein self-aggregation which is responsible for its toxic effect on Substantia nigra pars compacta and resultant neuronal death. Hence, blocking alpha-synuclein aggregation is a new channel to cure PD. This study initially investigates drug likeness and ADMET properties of CNB-001, 7,8 dihydroxyflavone, curcumin, naringenin and emodin and its inhibitory effect on alpha-synuclein (PDB: 1XQ8) aggregation via molecular docking (LeadIT). Results revealed that the ligands satisfy drug likeness and ADMET properties and best-fit ligands were associated with VAL95, GLU83 and ALA91 as major amino acid residues of receptor site. Moreover, CNB-001 showed potent inhibitory effect than other compounds with a docking score of –13.6158. Further, we investigated the inhibitory effect of CNB-001 against alpha-synuclein expression using MPTP induced Parkinson mice model. Results explicated and confirmed that CNB-001 inhibited α-synuclein expression significantly when compared to MPTP group as evinced by western blotting. Therefore, these results attribute that CNB-001 can be further developed as a promising therapeutic candidate for PD treatment.
{"title":"In silico identification of potent inhibitors of alpha-synuclein aggregation and its in vivo evaluation using MPTP induced Parkinson mice model","authors":"Richard L. Jayaraj, Namasivayam Elangovan","doi":"10.1016/j.biomag.2014.01.002","DOIUrl":"10.1016/j.biomag.2014.01.002","url":null,"abstract":"<div><p><span><span><span><span>Parkinson disease is a progressive </span>neurodegenerative disorder characterized by the presence of </span>Lewy bodies<span> with dense α-synuclein self-aggregation which is responsible for its toxic effect on Substantia nigra pars compacta and resultant neuronal death. Hence, blocking alpha-synuclein aggregation is a new channel to cure PD. This study initially investigates </span></span>drug<span><span> likeness and ADMET<span> properties of CNB-001, 7,8 dihydroxyflavone, curcumin<span>, naringenin and </span></span></span>emodin and its inhibitory effect on alpha-synuclein (PDB: </span></span><span>1XQ8</span><svg><path></path></svg><span>) aggregation via molecular docking<span><span> (LeadIT). Results revealed that the ligands satisfy drug likeness and ADMET properties and best-fit ligands were associated with VAL95, GLU83 and ALA91 as major amino acid residues of receptor site. Moreover, CNB-001 showed potent inhibitory effect than other compounds with a docking score of –13.6158. Further, we investigated the inhibitory effect of CNB-001 against alpha-synuclein expression using MPTP induced Parkinson mice model. Results explicated and confirmed that CNB-001 inhibited α-synuclein expression significantly when compared to MPTP group as evinced by </span>western blotting. Therefore, these results attribute that CNB-001 can be further developed as a promising therapeutic candidate for PD treatment.</span></span></p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 147-152"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.01.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"109516300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2014.01.003
Cátia Carvalho , Manuela Páris , Miguel Lemos , Bruno Peixoto
The recognition of emotions from facial expressions is a basic human aptitude. The aging process is related with a decrease of this ability, particularly in the recognition of negative emotions. This decrease is more prominent in the context of dementia. Despite the growing of researches on emotion recognition, there is a lack of instruments capable of identifying individual differences regarding aging and dementia. This work aims to determine the psychometric properties of a facial emotion recognition task (Gandra-BARTA). The sample is composed by three groups: Young Adults (YA) group (n = 12); Old Adults (OA) group (n = 17); Alzheimer's Disease (AD) group (n = 26), made up of subjects with diagnosis of probable AD. The Gandra-BARTA showed good internal consistency. In comparison to the YA, the OA group took more time to complete Gandra-BARTA, had less correct emotional identifications and they have under-recognized facial expressions of rage and neutral emotions. On the other hand, the AD group showed worst performance on every aspect of the Gandra-BARTA when compared to the OA group, except in the identification of sadness and fear. A cutoff score of 24 correct recognitions on Gandra-BARTA differentiate OA from AD subjects with a sensibility of 100% and a specificity of 88.5%. The Gandra-BARTA revealed good internal consistency making it a reliable instrument to assess the ability to recognize emotions from facial expressions. It also proved to be sensitive to changes in aging and dementia with high discriminant validity for AD.
{"title":"Assessment of facial emotions recognition in aging and dementia. The development of a new tool","authors":"Cátia Carvalho , Manuela Páris , Miguel Lemos , Bruno Peixoto","doi":"10.1016/j.biomag.2014.01.003","DOIUrl":"10.1016/j.biomag.2014.01.003","url":null,"abstract":"<div><p><span>The recognition of emotions from facial expressions is a basic human aptitude. The aging process is related with a decrease of this ability, particularly in the recognition of negative emotions. This decrease is more prominent in the context of dementia. Despite the growing of researches on emotion recognition, there is a lack of instruments capable of identifying individual differences regarding aging and dementia. This work aims to determine the psychometric properties of a facial emotion recognition task (Gandra-BARTA). The sample is composed by three groups: Young Adults (YA) group (</span><em>n</em> <!-->=<!--> <!-->12); Old Adults (OA) group (<em>n</em> <!-->=<!--> <span>17); Alzheimer's Disease (AD) group (</span><em>n</em> <!-->=<!--> <!-->26), made up of subjects with diagnosis of probable AD. The Gandra-BARTA showed good internal consistency. In comparison to the YA, the OA group took more time to complete Gandra-BARTA, had less correct emotional identifications and they have under-recognized facial expressions of rage and neutral emotions. On the other hand, the AD group showed worst performance on every aspect of the Gandra-BARTA when compared to the OA group, except in the identification of sadness and fear. A cutoff score of 24 correct recognitions on Gandra-BARTA differentiate OA from AD subjects with a sensibility of 100% and a specificity of 88.5%. The Gandra-BARTA revealed good internal consistency making it a reliable instrument to assess the ability to recognize emotions from facial expressions. It also proved to be sensitive to changes in aging and dementia with high discriminant validity for AD.</p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 91-94"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.01.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90578439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-01DOI: 10.1016/j.biomag.2014.02.002
Hong Guo , Yu Gao , Bin Gu , Jing Wang , Hongchen Liu
Objective
To investigate the antiosteoporotic effects of L-Arginine on ovariectomied rats.
Methods
Forty twelve-week-old female Sprague-Dawley rats were randomly divided into four groups of bilaterally ovariectomy and one group of Sham animals, with 8 animals in each group. Twelve additional weeks elapsed before initiation of the treatment with L-Arginine in order to induce significant bone loss in the ovariectomied animals. A 4-week daily treatment (5 days a week, Monday–Friday) at doses of 5 mg/kg/d, 10 mg/kg/d, 20 mg/kg/d of L-Arginine or vehicle only was administered by s.c. injection to the ovariectomied groups respectively. At the end of the treatment period, blood samples from all animals were collected for biochemical analysis. Micro-computerized tomography analysis, histopathological study and biomechanical test were performed on the femur of each animal.
Results
Serum alkaline phosphatase and osteocalcin were reduced in ovariectomied rats after the administration of different dosage of L-Arginine. L-Arginine of 10 mg/kg showed the most significant effect. Micro-computerized tomography 3-D images revealed that the increase of bone mass in 5 mg/kg and 10 mg/kg groups were significant greater than that in Sham group. The biomechanical parameters of femur were improved significantly in L-Arginine 10 mg/kg group when compared to untreated ovariectomied rats.
Conclusions
L-Arginine (10 mg/kg) contributes significantly to the treatment of the bone loss induced by ovariectomy on rats, demonstrated by increased bone mass, improved bone structure and recovery of bone biomechanical activity.
{"title":"Antiosteoporotic effects of L-Arginine in ovariectomied rats","authors":"Hong Guo , Yu Gao , Bin Gu , Jing Wang , Hongchen Liu","doi":"10.1016/j.biomag.2014.02.002","DOIUrl":"10.1016/j.biomag.2014.02.002","url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the antiosteoporotic effects of L-Arginine on ovariectomied rats.</p></div><div><h3>Methods</h3><p><span>Forty twelve-week-old female Sprague-Dawley rats were randomly divided into four groups of bilaterally ovariectomy<span> and one group of Sham animals, with 8 animals in each group. Twelve additional weeks elapsed before initiation of the treatment with L-Arginine in order to induce significant </span></span>bone loss<span> in the ovariectomied animals. A 4-week daily treatment (5 days a week, Monday–Friday) at doses of 5 mg/kg/d, 10 mg/kg/d, 20 mg/kg/d of L-Arginine or vehicle only was administered by s.c. injection to the ovariectomied groups respectively. At the end of the treatment period, blood samples from all animals were collected for biochemical analysis. Micro-computerized tomography analysis, histopathological study and biomechanical test were performed on the femur of each animal.</span></p></div><div><h3>Results</h3><p><span>Serum alkaline phosphatase and </span>osteocalcin were reduced in ovariectomied rats after the administration of different dosage of L-Arginine. L-Arginine of 10 mg/kg showed the most significant effect. Micro-computerized tomography 3-D images revealed that the increase of bone mass in 5 mg/kg and 10 mg/kg groups were significant greater than that in Sham group. The biomechanical parameters of femur were improved significantly in L-Arginine 10 mg/kg group when compared to untreated ovariectomied rats.</p></div><div><h3>Conclusions</h3><p>L-Arginine (10 mg/kg) contributes significantly to the treatment of the bone loss induced by ovariectomy on rats, demonstrated by increased bone mass, improved bone structure and recovery of bone biomechanical activity.</p></div>","PeriodicalId":100181,"journal":{"name":"Biomedicine & Aging Pathology","volume":"4 2","pages":"Pages 117-122"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biomag.2014.02.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76871255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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