Ivana Ponce, Cinthia Coria-lucero, M. G. Lacoste, M. C. Della Vedova, Cristina Devia, D. Ramirez, Sandra Gómez-mejiba, Silvia Marcela Delgado, Ana Anzulovich
Age impairs cognitive functions and antioxidant defenses, for example, by increasing oxidative stress and inflammation in the brain. However, so far, there is no report on the consequences of aging on temporal patterns of proteins and lipids oxidation, antioxidant enzymes activity, endogenous clock and proinflammatory cytokine, in the prefrontal cortex (PFC). Therefore, our objectives here were: 1) to investigate the endogenous nature of 24h-rhythms of lipoperoxidation, protein carbonyls levels, CAT and GPx activity, RORa, and TNFα, in the rat PFC, and 2) to study the consequences of aging on the circadian organization of those factors in the same brain area. To do that, 3- and 22-mo-old male Holtzman rats were maintained under constant darkness conditions during 15 days before reaching the corresponding age. PFC samples were isolated every 4 h, under dim-red light, during a 24h period. Our results revealed circadian patterns of antioxidant enzymes activity, oxidative stress, RORa and TNFα proteins levels, in the PFC of young rats. The circadian distribution of the rhythms’ phases suggests the existence of a reciprocal communication among the antioxidant defenses, the endogenous clock, and the inflammation, in the PFC. Noteworthy, such circadian organization disappears in the PFC of aged rats. An increased oxidative stress would make the redox environment to change into an oxidative status, which alters the endogenous clock activity and disrupts the circadian organization of, at least part, of the antioxidant defenses and the TNFα, in the PFC. These results might highlight novel chronobiological targets for the design of therapeutic strategies addressed to a healthy aging.
{"title":"Circadian rhythms of antioxidant enzymes activity, clock, and inflammation factors are disrupted in the prefrontal cortex of aged rats. Potential targets for therapeutic strategies for a healthy aging.","authors":"Ivana Ponce, Cinthia Coria-lucero, M. G. Lacoste, M. C. Della Vedova, Cristina Devia, D. Ramirez, Sandra Gómez-mejiba, Silvia Marcela Delgado, Ana Anzulovich","doi":"10.37212/jcnos.1460272","DOIUrl":"https://doi.org/10.37212/jcnos.1460272","url":null,"abstract":"Age impairs cognitive functions and antioxidant defenses, for example, by increasing oxidative stress and inflammation in the brain. However, so far, there is no report on the consequences of aging on temporal patterns of proteins and lipids oxidation, antioxidant enzymes activity, endogenous clock and proinflammatory cytokine, in the prefrontal cortex (PFC). Therefore, our objectives here were: 1) to investigate the endogenous nature of 24h-rhythms of lipoperoxidation, protein carbonyls levels, CAT and GPx activity, RORa, and TNFα, in the rat PFC, and 2) to study the consequences of aging on the circadian organization of those factors in the same brain area. To do that, 3- and 22-mo-old male Holtzman rats were maintained under constant darkness conditions during 15 days before reaching the corresponding age. PFC samples were isolated every 4 h, under dim-red light, during a 24h period. Our results revealed circadian patterns of antioxidant enzymes activity, oxidative stress, RORa and TNFα proteins levels, in the PFC of young rats. The circadian distribution of the rhythms’ phases suggests the existence of a reciprocal communication among the antioxidant defenses, the endogenous clock, and the inflammation, in the PFC. Noteworthy, such circadian organization disappears in the PFC of aged rats. An increased oxidative stress would make the redox environment to change into an oxidative status, which alters the endogenous clock activity and disrupts the circadian organization of, at least part, of the antioxidant defenses and the TNFα, in the PFC. These results might highlight novel chronobiological targets for the design of therapeutic strategies addressed to a healthy aging.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141662950","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}
Fajri Ramadhan Marviano, Putra Santoso, Resti Rahayu
The transformation of our era, resulting in a change in dietary habits towards a higher intake of fatty foods, presents a worldwide health issue. Among these challenges is neurodegeneration, which leads to cognitive impairment. It is imperative to seek alternative solutions rooted in nature to address the limitations associated with non-natural treatment methods. This entails harnessing the properties of secondary metabolite compounds found in plants, such as Colocasia esculenta Var. Mentawai. This research aims to assess the efficacy of C. esculenta Var. Mentawai corm as neuroprotective agents in mitigating CNS damage and preventing cognitive decline associated with neurodegeneration. Daily administration of a high-fat diet and a mixture of taro flour is conducted on young adult male mice for a duration of 60 days. Furthermore, analysis of the neurocognitive ability of mice, determination of malondialdehyde levels, and observation of histopathological structures on brain tissue were carried out. The results showed that the group of mice fed with taro flour mixture effectively showed a positive impact on maintaining neurocognitive abilities and histopathological structure of brain tissue against neurodegeneration (p
{"title":"Neuroprotective Effect of Colocasia esculenta Var. Mentawai Corm Flour High-Fat Diet Fed Mice","authors":"Fajri Ramadhan Marviano, Putra Santoso, Resti Rahayu","doi":"10.37212/jcnos.1470198","DOIUrl":"https://doi.org/10.37212/jcnos.1470198","url":null,"abstract":"The transformation of our era, resulting in a change in dietary habits towards a higher intake of fatty foods, presents a worldwide health issue. Among these challenges is neurodegeneration, which leads to cognitive impairment. It is imperative to seek alternative solutions rooted in nature to address the limitations associated with non-natural treatment methods. This entails harnessing the properties of secondary metabolite compounds found in plants, such as Colocasia esculenta Var. Mentawai. This research aims to assess the efficacy of C. esculenta Var. Mentawai corm as neuroprotective agents in mitigating CNS damage and preventing cognitive decline associated with neurodegeneration. Daily administration of a high-fat diet and a mixture of taro flour is conducted on young adult male mice for a duration of 60 days. Furthermore, analysis of the neurocognitive ability of mice, determination of malondialdehyde levels, and observation of histopathological structures on brain tissue were carried out. The results showed that the group of mice fed with taro flour mixture effectively showed a positive impact on maintaining neurocognitive abilities and histopathological structure of brain tissue against neurodegeneration (p","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141663584","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}
Migraine is a complex neurological problem whose primary symptom is headache and is common in the human population. It is well known that neuroinflammation plays a vital role in the pathogenesis of migraine, with adverse effects on the nervous system, including headache disorders such as migraine. The infusion of the nitric oxide donor glyceryl trinitrate (GTN) is often used in experimental models of migraine because it is the best-known model of migraine provocation. N-(p-amyl cinnamoyl) anthranilic acid (ACA) has been shown to inhibit both TRPM2 and phospholipase A2 (PLA2). Recent research has explored potential interventions to mitigate GTN-induced neurotoxicity. One such candidate is ACA, a compound with anti-inflammatory and antioxidant properties.
Thirty-six C57BL/6j black mice were divided into the control groups of ACA, GTN, and ACA+GTN. Mice in the ACA were treated intraperitoneally with ACA (25 mg/kg) for three days. Mice in the GTN were treated intraperitoneally with a single dose of GTN (10 mg/kg) for migraine induction. After the experimental stages were completed, the mice in all groups were sacrificed, and brain tissue and erythrocyte samples were taken from the mice.
The levels of inflammatory cytokines (TNF α, IL 1β, and IL 6), apoptosis, intracellular ROS, lipid peroxidation, caspase 3-9, and mitochondrial membrane potential increased in the GTN group. However, their levels were decreased in the ACA+GTN group by the injection of ACA. The treatment of ACA regulated the GTN treatment-induced decreases of glutathione levels, glutathione peroxidase activation, and cell viability in the brain and erythrocytes.
In conclusion, GTN plays a role in neurotoxicity caused by increased apoptosis and ROS. We observed that ACA modulated the brain and erythrocyte oxidant, antioxidant parameters, and apoptotic processes. The neuro-protective role of ACA treatment may be explained by its modulating activity against increased apoptosis and oxidative stress.
{"title":"Regulatory role of phospholipase A2 inhibitor in oxidative stress and inflammation induced by an experimental mouse migraine model","authors":"Betül YAZĞAN, Yener YAZĞAN","doi":"10.37212/jcnos.1365512","DOIUrl":"https://doi.org/10.37212/jcnos.1365512","url":null,"abstract":"Migraine is a complex neurological problem whose primary symptom is headache and is common in the human population. It is well known that neuroinflammation plays a vital role in the pathogenesis of migraine, with adverse effects on the nervous system, including headache disorders such as migraine. The infusion of the nitric oxide donor glyceryl trinitrate (GTN) is often used in experimental models of migraine because it is the best-known model of migraine provocation. N-(p-amyl cinnamoyl) anthranilic acid (ACA) has been shown to inhibit both TRPM2 and phospholipase A2 (PLA2). Recent research has explored potential interventions to mitigate GTN-induced neurotoxicity. One such candidate is ACA, a compound with anti-inflammatory and antioxidant properties.
 Thirty-six C57BL/6j black mice were divided into the control groups of ACA, GTN, and ACA+GTN. Mice in the ACA were treated intraperitoneally with ACA (25 mg/kg) for three days. Mice in the GTN were treated intraperitoneally with a single dose of GTN (10 mg/kg) for migraine induction. After the experimental stages were completed, the mice in all groups were sacrificed, and brain tissue and erythrocyte samples were taken from the mice.
 The levels of inflammatory cytokines (TNF α, IL 1β, and IL 6), apoptosis, intracellular ROS, lipid peroxidation, caspase 3-9, and mitochondrial membrane potential increased in the GTN group. However, their levels were decreased in the ACA+GTN group by the injection of ACA. The treatment of ACA regulated the GTN treatment-induced decreases of glutathione levels, glutathione peroxidase activation, and cell viability in the brain and erythrocytes.
 In conclusion, GTN plays a role in neurotoxicity caused by increased apoptosis and ROS. We observed that ACA modulated the brain and erythrocyte oxidant, antioxidant parameters, and apoptotic processes. The neuro-protective role of ACA treatment may be explained by its modulating activity against increased apoptosis and oxidative stress.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135133408","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}
Ferroptosis is a non-apoptotic cell death closely related to a metabolic pathway involving iron overload, imbalanced glutathione metabolism, oxidative stress and lipid peroxidation damage. Obesity is closely associated with these imbalances. In this study, we aimed to investigate the effect of hippocampal ferroptosis in an obesity model and the potential role of N-acetylcysteine (NAC) against ferroptosis. A high-fat (60%) dietary pattern was used to establish an obesity model for 15 weeks. NAC was administered to NAC and Obese+NAC (ObNAC) groups by oral gavage at a dose of 150 mg/kg for 3 weeks. Glutathione peroxidase 4 (GPX4) and the cystine transporter solute carrier family 7- member 11 (SLC7A11) expression levels were investigated immunohistochemically to detect ferroptosis in hippocampal tissues. In the statistical analysis, H-scores of GPX4 and SLC7A11 in the hippocampus sections of the Ob group were significantly lower than in the control, NAC and ObNAC groups (p
{"title":"Protective effect of N-acetylcysteine on hippocampal ferroptosis in an experimental obesity model","authors":"Kiymet Kubra TÜFEKCİ, Musa TATAR","doi":"10.37212/jcnos.1358141","DOIUrl":"https://doi.org/10.37212/jcnos.1358141","url":null,"abstract":"Ferroptosis is a non-apoptotic cell death closely related to a metabolic pathway involving iron overload, imbalanced glutathione metabolism, oxidative stress and lipid peroxidation damage. Obesity is closely associated with these imbalances. In this study, we aimed to investigate the effect of hippocampal ferroptosis in an obesity model and the potential role of N-acetylcysteine (NAC) against ferroptosis. A high-fat (60%) dietary pattern was used to establish an obesity model for 15 weeks. NAC was administered to NAC and Obese+NAC (ObNAC) groups by oral gavage at a dose of 150 mg/kg for 3 weeks. Glutathione peroxidase 4 (GPX4) and the cystine transporter solute carrier family 7- member 11 (SLC7A11) expression levels were investigated immunohistochemically to detect ferroptosis in hippocampal tissues. In the statistical analysis, H-scores of GPX4 and SLC7A11 in the hippocampus sections of the Ob group were significantly lower than in the control, NAC and ObNAC groups (p","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135133407","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}
Diabetes, which causes oxidative stress-induced neuronal damage, is still one of the most important chronic health problems in the world. It can cause serious cellular loss and damage throughout the course of the disease. It is hypothesized that increased oxidative stress in this process increases free reactive oxygen species (ROS) and apoptotic markers and causes diabetic damage. Alpha-Lipoic acid (α-LA), which has a direct antioxidant effect in ROS reduction reactions, is also among the main components of the antioxidant system that works for free radical control and apoptosis. To understand the role of α-LA in reducing diabetes-induced oxidative damage, we examined the production of ROS in the brain cortex and erythrocytes of rats and their effects on markers of apoptosis. Forty adult Wistar albino rats were divided into four groups as control, α-LA, diabetic (DIA), and DIA+α-LA. For the induction of diabetes, the intraperitoneal injection of a dose of streptozotocin (STZ) (45 mg/kg) was used. α-LA (50 mg/kg) was applied to the groups of α-LA and DIA+α-LA for 14 days. At the end of the experiment, the brain cortex tissue and erythrocyte samples were taken from the rats. The levels of apoptosis, caspase 3, caspase 9, mitochondrial membrane potential, intracellular ROS, and lipid peroxidation were increased in the STZ group, although their levels were decreased in the DIA+α-LA group by the injection of α-LA. The STZ treatmentinduced decreases of cell viability, reduced glutathione, and glutathione peroxidase were increased in the brain and erythrocytes by the treatment of α-LA. In conclusion, diabetes acted a role in neuronal damage caused by increased ROS and apoptosis. We observed that α-LA induced a modulatory role on the apoptotic, oxidant, and antioxidant parameters in the brain and erythrocyte. The neuroprotective role of α-LA treatment may be explained by its modulating activity against increased oxidative stress and apoptosis.
{"title":"Potent antioxidant alpha lipoic acid reduces STZ-induced oxidative stress and apoptosis levels in the erythrocytes and brain cells of diabetic rats","authors":"Betul Yazğan, Y. Yazğan","doi":"10.37212/jcnos.1245152","DOIUrl":"https://doi.org/10.37212/jcnos.1245152","url":null,"abstract":"Diabetes, which causes oxidative stress-induced neuronal damage, is still one of the most important chronic health problems in the world. It can cause serious cellular loss and damage throughout the course of the disease. It is hypothesized that increased oxidative stress in this process increases free reactive oxygen species (ROS) and apoptotic markers and causes diabetic damage. Alpha-Lipoic acid (α-LA), which has a direct antioxidant effect in ROS reduction reactions, is also among the main components of the antioxidant system that works for free radical control and apoptosis. To understand the role of α-LA in reducing diabetes-induced oxidative damage, we examined the production of ROS in the brain cortex and erythrocytes of rats and their effects on markers of apoptosis.\u0000 Forty adult Wistar albino rats were divided into four groups as control, α-LA, diabetic (DIA), and DIA+α-LA. For the induction of diabetes, the intraperitoneal injection of a dose of streptozotocin (STZ) (45 mg/kg) was used. α-LA (50 mg/kg) was applied to the groups of α-LA and DIA+α-LA for 14 days. At the end of the experiment, the brain cortex tissue and erythrocyte samples were taken from the rats.\u0000 The levels of apoptosis, caspase 3, caspase 9, mitochondrial membrane potential, intracellular ROS, and lipid peroxidation were increased in the STZ group, although their levels were decreased in the DIA+α-LA group by the injection of α-LA. The STZ treatmentinduced decreases of cell viability, reduced glutathione, and glutathione peroxidase were increased in the brain and erythrocytes by the treatment of α-LA. \u0000 In conclusion, diabetes acted a role in neuronal damage caused by increased ROS and apoptosis. We observed that α-LA induced a modulatory role on the apoptotic, oxidant, and antioxidant parameters in the brain and erythrocyte. The neuroprotective role of α-LA treatment may be explained by its modulating activity against increased oxidative stress and apoptosis.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47270220","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}
Diana Monge-Sanchez, M. Montiel-Herrera, Denısse GARCİA VİLLA, Guillermo Lopez, J. A. Domínguez-Avila, G. González-Aguilar
Classic non-homeostatic structures involved in food intake regulation are reciprocally influenced by metabolic signals. Orexigenic peptides expressed in the olfactory bulb (OB) and hippocampus (HP) modulate olfactory processing and memory, respectively. Hypothalamic circuits also modulate feeding behavior by activating and releasing Agouti-related peptide (AgRP) in response to orexigenic signals. An adequate response to fasting requires the expression of p75 neurotrophin receptor (p75NTR) in AgRP neurons. The present study aimed to determine whether there is a role for p75NTR and AgRP in the OB and HP on the feeding behavior of fasted rats. A group of fasted rats (FG) was confronted with a decision-making paradigm in a T-maze containing a standard chow pellet (CP), and the same pellet coated with a phenolic-rich avocado paste extract (AVO) on either end; their OB and HP were then analyzed with histological and molecular tools. FG rats had briefer feeding latencies, as compared to control rats fed ad libitum (median latencies: 55.4 vs 191.7 min, p = 0.032). They also had reduced cell counts in both brain structures, as compared to satiated rats. AgRP mRNA was not expressed in the HP of either group, however, it was found in the OB. p75NTR mRNA was expressed in both brain structures of FG rats. These results suggest that contrasting metabolic states (fasted or satiated) motivate different feeding responses, which are influenced by p75NTR and AgRP mRNA expression in non-homeostatic food intake brain structures.
参与食物摄入调节的经典非稳态结构受到代谢信号的相互影响。在嗅球(OB)和海马(HP)中表达的致氧肽分别调节嗅觉加工和记忆。下丘脑回路也通过激活和释放agouti相关肽(AgRP)来调节摄食行为，以响应摄氧信号。对禁食的充分反应需要AgRP神经元中p75神经营养因子受体(p75NTR)的表达。本研究旨在确定OB和HP中的p75NTR和AgRP是否对禁食大鼠的摄食行为有影响。一组禁食大鼠(FG)在t型迷宫中面临决策范式，其中含有标准鼠粮颗粒(CP)，同一鼠粮颗粒的两端涂有富含酚的鳄梨酱提取物(AVO);然后用组织学和分子工具分析OB和HP。与自由喂养的对照组大鼠相比，FG大鼠的进食潜伏期更短(中位潜伏期:55.4 vs 191.7 min, p = 0.032)。与吃饱的大鼠相比，它们的两个大脑结构中的细胞计数也减少了。AgRP mRNA在两组大鼠HP中均未表达，但在ob中均有表达。p75NTR mRNA在FG大鼠的两个脑结构中均有表达。这些结果表明，不同的代谢状态(禁食或饱食)激发了不同的摄食反应，这些反应受非稳态食物摄入脑结构中p75NTR和AgRP mRNA表达的影响。
{"title":"Fasting alters p75NTR and AgRP mRNA expression in rat olfactory bulb and hippocampus","authors":"Diana Monge-Sanchez, M. Montiel-Herrera, Denısse GARCİA VİLLA, Guillermo Lopez, J. A. Domínguez-Avila, G. González-Aguilar","doi":"10.37212/jcnos.1168800","DOIUrl":"https://doi.org/10.37212/jcnos.1168800","url":null,"abstract":"Classic non-homeostatic structures involved in food intake regulation are reciprocally influenced by metabolic signals. Orexigenic peptides expressed in the olfactory bulb (OB) and hippocampus (HP) modulate olfactory processing and memory, respectively. Hypothalamic circuits also modulate feeding behavior by activating and releasing Agouti-related peptide (AgRP) in response to orexigenic signals. An adequate response to fasting requires the expression of p75 neurotrophin receptor (p75NTR) in AgRP neurons. The present study aimed to determine whether there is a role for p75NTR and AgRP in the OB and HP on the feeding behavior of fasted rats. A group of fasted rats (FG) was confronted with a decision-making paradigm in a T-maze containing a standard chow pellet (CP), and the same pellet coated with a phenolic-rich avocado paste extract (AVO) on either end; their OB and HP were then analyzed with histological and molecular tools. FG rats had briefer feeding latencies, as compared to control rats fed ad libitum (median latencies: 55.4 vs 191.7 min, p = 0.032). They also had reduced cell counts in both brain structures, as compared to satiated rats. AgRP mRNA was not expressed in the HP of either group, however, it was found in the OB. p75NTR mRNA was expressed in both brain structures of FG rats. These results suggest that contrasting metabolic states (fasted or satiated) motivate different feeding responses, which are influenced by p75NTR and AgRP mRNA expression in non-homeostatic food intake brain structures.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41328374","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}
Aluminum chloride (AlCl3) causes neuroinflammation in rats, which leads to the development of Alzheimer's disease. The current study focused on the anti-Alzheimer and antioxidant potential of hydromethanolic extracts of Pluchea lanceolata (PL), a well-known Rasna source. Phytoconstituents such as pluchine and moretenol acetate are selected for the PASS online and molecular docking (in silico) experimental model. A total of 36 Wistar rats were divided into VI groups, each with six rats. Group I: normal control, Group II: disease control, Group III: Rivastigmine (0.3 mg/kg, p.o), Group IV and V: Hydromethanolic extract of PL (HMEPL, 200 mg/kg, 400 mg/kg, p.o), and Group VI: Ayurvedic Formulation of Rasna (AFR) (1ml/kg, p.o). Except for group I, all of the animals were given Aluminum Chloride (AlCl3) (300 mg/kg, p.o). AlCl3 and plant extracts were given for 20day treatment. On the 0th, 7th, 14th, and 20th days, the behavioural study and changes in body weight were evaluated. Rats were sacrificed on the 21st day, their brains were separated, and antioxidant enzyme levels, protein levels, and neurotransmitter levels were measured. Histopathologies of the cortex and hippocampus parts of the brain were studied. The number of entries, as well as time spent in the closed arm and time taken to ascend the pole, were all increased in Group II animals, but this was reversed in groups treated with 200 mg/kg, 400 mg/kg, and1 ml/kg dosages of HMEPL and AFR. In the disease control group, AlCl3 (300 mg/kg, p.o.) caused a 1.5 fold increase in protein content and 1.7 fold increase in malondialdehyde, similarly, 1.3 fold reduction in body weight, 2.2 fold superoxide dismutase, 3.3 fold catalase, and 3.1 fold glutathione level were observed and were corrected and restored in groups treated with HMEPL and AFR. Furthermore, the histopathology findings revealed that HMEPL and AFR provided the cellular-level protection. The active components of HMEPL were found to have anti-Alzheimer and antioxidant potential and were confirmed in an in silico investigation. HMEPL > AFR was the order of anti-Alzheimer and antioxidant effectiveness.
{"title":"The beneficial effect of Pluchea lanceolata on aluminum chloride-induced Alzheimer's disease in rats","authors":"Raju Asirvatham, Daiay Pa, S. Salam","doi":"10.37212/jcnos.1117261","DOIUrl":"https://doi.org/10.37212/jcnos.1117261","url":null,"abstract":"Aluminum chloride (AlCl3) causes neuroinflammation in rats, which leads to the development of Alzheimer's disease. The current study focused on the anti-Alzheimer and antioxidant potential of hydromethanolic extracts of Pluchea lanceolata (PL), a well-known Rasna source. Phytoconstituents such as pluchine and moretenol acetate are selected for the PASS online and molecular docking (in silico) experimental model. A total of 36 Wistar rats were divided into VI groups, each with six rats. Group I: normal control, Group II: disease control, Group III: Rivastigmine (0.3 mg/kg, p.o), Group IV and V: Hydromethanolic extract of PL (HMEPL, 200 mg/kg, 400 mg/kg, p.o), and Group VI: Ayurvedic Formulation of Rasna (AFR) (1ml/kg, p.o). Except for group I, all of the animals were given Aluminum Chloride (AlCl3) (300 mg/kg, p.o). AlCl3 and plant extracts were given for 20day treatment. On the 0th, 7th, 14th, and 20th days, the behavioural study and changes in body weight were evaluated. Rats were sacrificed on the 21st day, their brains were separated, and antioxidant enzyme levels, protein levels, and neurotransmitter levels were measured. Histopathologies of the cortex and hippocampus parts of the brain were studied. The number of entries, as well as time spent in the closed arm and time taken to ascend the pole, were all increased in Group II animals, but this was reversed in groups treated with 200 mg/kg, 400 mg/kg, and1 ml/kg dosages of HMEPL and AFR. In the disease control group, AlCl3 (300 mg/kg, p.o.) caused a 1.5 fold increase in protein content and 1.7 fold increase in malondialdehyde, similarly, 1.3 fold reduction in body weight, 2.2 fold superoxide dismutase, 3.3 fold catalase, and 3.1 fold glutathione level were observed and were corrected and restored in groups treated with HMEPL and AFR. Furthermore, the histopathology findings revealed that HMEPL and AFR provided the cellular-level protection. The active components of HMEPL were found to have anti-Alzheimer and antioxidant potential and were confirmed in an in silico investigation. HMEPL > AFR was the order of anti-Alzheimer and antioxidant effectiveness.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44210842","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}
Alzheimer’s disease is a common neurodegenerative disease. Microglia induces oxidative stress in the brain for engulfing bacteria and viruses. The accumulating data indicate that oxidative stress and apoptosis are two main actors for the induction of microglia activation-induced Alzheimer’s Disease. Oxidative stress is one of many triggers that activate the transient receptor potential melastatin 2 (TRPM2) channel. Glutathione (GSH) is a main cytosolic antioxidant in the mammalian cells. The GSH depletion via the activation of TRPM2 induces oxidative stress and apoptosis in neuronal cells. It has not yet been researched how GSH depletion via activation of TRPM2 affects oxidative stress and apoptosis in microglial cells with the Alzheimer's disease model. The BV2 cells divided into 5 groups as control, buthionine sulphoximine (BSO and 0.5 mM for 6 h), amyloid beta (1 uM for 72 h), amyloid beta+BSO, and amyloid beta+BSO+GSH (10 mM for 2 h). In the BSO group, the levels of apoptosis, mitochondrial membrane potential, cytosolic free oxygen reactive species (cyROS), caspase (Casps) -3, Casps -8, and Casps -9 were increased as compared to the control group, although cell viability level was decreased. The expression levels of TRPM2, Casps -3, Casps -9, Bax, Bcl-2, and PARP-1 were also increased in the BSO group. In addition, their levels were further increased in the amyloid beta and BSO+amyloid beta groups as compared to the BSO group. However, the changes were modulated in the BSO+amyloid beta+GSH group by the incubation of GSH. In conclusion, the depletion of GSH increased apoptosis and cyROS levels via activation of caspases and TRPM2 in the amyloid beta-induced microglia cells. The treatment of GSH may be a potential target on the apoptosis and oxidative stress in the amyloid beta-induced microglia cells.
{"title":"Depletion of glutathione induced apoptosis and oxidative stress via the activation of TRPM2 channels in the microglia cells with Alzheimer’ disease model","authors":"Ramazan Çınar","doi":"10.37212/jcnos.1147935","DOIUrl":"https://doi.org/10.37212/jcnos.1147935","url":null,"abstract":"Alzheimer’s disease is a common neurodegenerative disease. Microglia induces oxidative stress in the brain for engulfing bacteria and viruses. The accumulating data indicate that oxidative stress and apoptosis are two main actors for the induction of microglia activation-induced Alzheimer’s Disease. Oxidative stress is one of many triggers that activate the transient receptor potential melastatin 2 (TRPM2) channel. Glutathione (GSH) is a main cytosolic antioxidant in the mammalian cells. The GSH depletion via the activation of TRPM2 induces oxidative stress and apoptosis in neuronal cells. It has not yet been researched how GSH depletion via activation of TRPM2 affects oxidative stress and apoptosis in microglial cells with the Alzheimer's disease model. The BV2 cells divided into 5 groups as control, buthionine sulphoximine (BSO and 0.5 mM for 6 h), amyloid beta (1 uM for 72 h), amyloid beta+BSO, and amyloid beta+BSO+GSH (10 mM for 2 h). In the BSO group, the levels of apoptosis, mitochondrial membrane potential, cytosolic free oxygen reactive species (cyROS), caspase (Casps) -3, Casps -8, and Casps -9 were increased as compared to the control group, although cell viability level was decreased. The expression levels of TRPM2, Casps -3, Casps -9, Bax, Bcl-2, and PARP-1 were also increased in the BSO group. In addition, their levels were further increased in the amyloid beta and BSO+amyloid beta groups as compared to the BSO group. However, the changes were modulated in the BSO+amyloid beta+GSH group by the incubation of GSH. In conclusion, the depletion of GSH increased apoptosis and cyROS levels via activation of caspases and TRPM2 in the amyloid beta-induced microglia cells. The treatment of GSH may be a potential target on the apoptosis and oxidative stress in the amyloid beta-induced microglia cells.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44013671","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}
7th Brain Research School (2022-BRS) was performed in Isparta, Turkey between 27 June and 3 July 2022 (http://2022.brs.org.tr/). There were abstracts of 8 speakers, 11 oral presentations, and 3 poster presentations in the 2022-BRS. Titles of speakers; 1- Mustafa NAZIROĞLU. Fluorescent Ca2+ stains for imaging the mice microglia. 2- Beatrice Mihaela RADU. Low-energy accelerated protons irradiation inhibits DNA repair and diminishes cell proliferation, migration and calcium signaling in brain microvascular endothelial cells. 3- Nashat ABUMARIA. Behavioral assays and animal models of psychiatric disorders. 4- Ferah YILDIRIM. Mapping genome-wide DNA methylation changes in alcohol use disorder (No abstrcat). 5- Marco CANEPARI. Principles of Ca2+ imaging using low-affinity indicators. 6- Denis ROUSSEAU. Western blot analyses in the mitochondria. 7- Xinhua SHU. Protection of p-Coumaric acid against depression and memory impairment via inhibition of neuroinflammation 8- Simon HEBEISEN. State dependent block of voltage gated sodium and calcium channels as modern treatment for epilepsy. Titles of oral presentations (OPs); OP1. Bünyamin AYDIN. Diabetic neuropathic pain and TRPM2 Channel: Focus on selenium. OP2. Agomelatine attenuates calcium signaling and apoptosis via the inhibition of TRPV1 channel in the hippocampal neurons of rats with chronic mild stress depression model. OP3. Hatice DALDAL. An interaction between cisplatin-induced optic nerve injury and TRPM2 channel. OP4. Kemal ERTİLAV. Recent developments on the traumatic brain injury models in the experimental animals. OP5. Kaan ERBAKAN. Involvement of TRPV1 channel in the etiology of epilepsy. OP6. Ramazan ÇINAR. Does GSH depletion induce TRPM2 activation in neuronal cells? OP7. Esin AKBAY ÇETİN. TRP ion channels and approaches in COVID-19. OP8. Gülin ÖZDAMAR ÜNAL. Early life stress and neuroinflammation. OP9. Adem AHLATCI. Investigation of TRPM2 cation channel activation in PTZ-induced SH-SY5Y cells by patch-clamp technique: Regulatory role of valproic acid. OP10. Yener YAZĞAN. Orthodontic teeth movement-induced pain and TRPV1 channel. OP11. Evaluation of the role of Radish (Raphanus sativus) extract in movement tests in MPTP induced experimental Parkinson's model in Balb/C mice. Titles of poster presentations (P); P1- Esin AKBAY ÇETİN. Probable pathways of SARS-CoV-2 to central nervous system. P2. Yusuf DAL. Low molecular weight heparin treatment reduced apoptosis, oxidative stress, and calcium signaling in the thrombocytes of patients with recurrent pregnancy loss and thrombophilia: Involvements of TRPM2 and TRPV1 channels. P3. Ferruh KARAMANGİL. Investigation of frequency and diversity of experimental animal models of schizophrenia.
{"title":"Abstract Book of 7th Brain Research School (2022-BRS), 27 June and 3 July 2022, Isparta, Turkey (http://2022.brs.org.tr/)","authors":"Anonymes ABSTRACT BOOK","doi":"10.37212/jcnos.1143834","DOIUrl":"https://doi.org/10.37212/jcnos.1143834","url":null,"abstract":"7th Brain Research School (2022-BRS) was performed in Isparta, Turkey between 27 June and 3 July 2022 (http://2022.brs.org.tr/). There were abstracts of 8 speakers, 11 oral presentations, and 3 poster presentations in the 2022-BRS.\u0000Titles of speakers;\u00001- Mustafa NAZIROĞLU. Fluorescent Ca2+ stains for imaging the mice microglia.\u00002- Beatrice Mihaela RADU. Low-energy accelerated protons irradiation inhibits DNA repair and diminishes cell proliferation, migration and calcium signaling in brain microvascular endothelial cells.\u00003- Nashat ABUMARIA. Behavioral assays and animal models of psychiatric disorders.\u00004- Ferah YILDIRIM. Mapping genome-wide DNA methylation changes in alcohol use disorder (No abstrcat).\u00005- Marco CANEPARI. Principles of Ca2+ imaging using low-affinity indicators.\u00006- Denis ROUSSEAU. Western blot analyses in the mitochondria.\u00007- Xinhua SHU. Protection of p-Coumaric acid against depression and memory impairment via inhibition of neuroinflammation\u00008- Simon HEBEISEN. State dependent block of voltage gated sodium and calcium channels as modern treatment for\u0000epilepsy.\u0000\u0000Titles of oral presentations (OPs);\u0000OP1. Bünyamin AYDIN. Diabetic neuropathic pain and TRPM2 Channel: Focus on selenium.\u0000OP2. Agomelatine attenuates calcium signaling and apoptosis via the inhibition of TRPV1\u0000channel in the hippocampal neurons of rats with chronic mild stress depression model.\u0000OP3. Hatice DALDAL. An interaction between cisplatin-induced optic nerve injury and TRPM2 channel.\u0000OP4. Kemal ERTİLAV. Recent developments on the traumatic brain injury models in the experimental animals.\u0000OP5. Kaan ERBAKAN. Involvement of TRPV1 channel in the etiology of epilepsy.\u0000OP6. Ramazan ÇINAR. Does GSH depletion induce TRPM2 activation in neuronal cells?\u0000OP7. Esin AKBAY ÇETİN. TRP ion channels and approaches in COVID-19.\u0000OP8. Gülin ÖZDAMAR ÜNAL. Early life stress and neuroinflammation.\u0000OP9. Adem AHLATCI. Investigation of TRPM2 cation channel activation in PTZ-induced SH-SY5Y cells by patch-clamp technique: Regulatory role of valproic acid.\u0000OP10. Yener YAZĞAN. Orthodontic teeth movement-induced pain and TRPV1 channel.\u0000OP11. Evaluation of the role of Radish (Raphanus sativus) extract in movement tests in MPTP induced experimental Parkinson's model in Balb/C mice.\u0000\u0000Titles of poster presentations (P);\u0000P1- Esin AKBAY ÇETİN. Probable pathways of SARS-CoV-2 to central nervous system.\u0000P2. Yusuf DAL. Low molecular weight heparin treatment reduced apoptosis, oxidative stress, and calcium signaling in the thrombocytes of patients with recurrent pregnancy loss and thrombophilia: Involvements of TRPM2 and TRPV1 channels.\u0000P3. Ferruh KARAMANGİL. Investigation of frequency and diversity of experimental animal models of schizophrenia.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46110618","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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