Metabolic brain disease最新文献_第7页

Neuroprotective efficacy of Talinum triangulare in Cadmium-induced neurotoxicity: involvement of antioxidant defense, anti-inflammatory, dopaminergic, and cholinergic systems. 三角Talinum对镉诱导的神经毒性的神经保护作用：涉及抗氧化防御、抗炎、多巴胺和胆碱能系统。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-30 DOI: 10.1007/s11011-025-01655-1

Johnson O Oladele, Ebenezer I O Ajayi, Isaac O Babatunde, Olaide O Awosanya, Oluwaseun T Oladele, Oluwafemi S Atolagbe, Omowumi O Adewale, Oyedotun M Oyeleke

{"title":"Neuroprotective efficacy of Talinum triangulare in Cadmium-induced neurotoxicity: involvement of antioxidant defense, anti-inflammatory, dopaminergic, and cholinergic systems.","authors":"Johnson O Oladele, Ebenezer I O Ajayi, Isaac O Babatunde, Olaide O Awosanya, Oluwaseun T Oladele, Oluwafemi S Atolagbe, Omowumi O Adewale, Oyedotun M Oyeleke","doi":"10.1007/s11011-025-01655-1","DOIUrl":"10.1007/s11011-025-01655-1","url":null,"abstract":"The incidence of neurotoxicity has been rising recently due to increase exposure to toxic compounds such as Cadmium (Cd). Aqueous leaf extract of Talinum triangulare (AETT) is used in traditional medicine in the treatment of various kinds of diseases. This study sought to examine neuroprotective potential of AETT on cadmium-induced neurotoxicity in rats. Neurotoxicity was induced in rats via oral administration of 5 mg/kg body weight CdCl2 and treated with either 200 mg/kg of AETT or vitamin E for 14 consecutive days. Results revealed that Cd induced behavioural incompetence with marked decrease in motor skills, muscle strength, exploratory activities, and anxiogenic-like phenotype which are vital psychomotor coordination tools. Cd intoxication caused a marked increase in neuronal expression of inflammatory biomarkers (TNF-α, MPO and NO), hydrogen peroxide generation, and lipid peroxidation; with associated decrease in both enzymatic antioxidants (GST, SOD, CAT) and non-enzymatic antioxidants (reduced glutathione). Similarly, decreased in dopamine with concomitant increased in the activity of acetylcholinesterase were observed in Cd-induced rats. Nevertheless, AETT or vitamin E markedly restored behavioural competence, mitigated neuroinflammation, lipid peroxidation and oxidative stress. AETT modulated cholinergic and dopaminergic pathways which improved bioavailability of acetylcholine and dopamine in the brain. Furthermore, AETT displayed better protective effects than vitamin E, this could be because of antioxidant phytochemicals in AETT as showed in the GCMS result. Overall, this study suggested AETT as a potential therapeutic agent in the treatment of neurotoxicity mediated by toxic metals.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"237"},"PeriodicalIF":3.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanisms of SIRT1/SIRT3-mediated reduction of mitochondrial regeneration and inflammatory response in diabetic cerebral ischemia-reperfusion injury. SIRT1/ sirt3介导的糖尿病脑缺血再灌注损伤中线粒体再生和炎症反应减少的机制

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-28 DOI: 10.1007/s11011-025-01662-2

Cheng Xin, Ouya Liu, Miao Sun, Ping Han, Xiaowen Li, Qingfeng Niu, Nenghong Ma, Xiao Yang, Changchun Hei, Ping Liu

引用次数: 0

Association between traumatic brain injury and risk of developing infections in the central nervous system and periphery. 创伤性脑损伤与中枢神经系统和外周神经系统感染风险之间的关系。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-26 DOI: 10.1007/s11011-025-01658-y

Cristiano Julio Faller, Amanda C S Kursancew, Beatriz Brandão Lima, Nicole Golombieski Duarte, Júlia Torcelli Noetzold, Natalli Studnicka, Khiany Mathias, Fabricia Petronilho, Emilio Luiz Streck, Jaqueline S Generoso

{"title":"Association between traumatic brain injury and risk of developing infections in the central nervous system and periphery.","authors":"Cristiano Julio Faller, Amanda C S Kursancew, Beatriz Brandão Lima, Nicole Golombieski Duarte, Júlia Torcelli Noetzold, Natalli Studnicka, Khiany Mathias, Fabricia Petronilho, Emilio Luiz Streck, Jaqueline S Generoso","doi":"10.1007/s11011-025-01658-y","DOIUrl":"10.1007/s11011-025-01658-y","url":null,"abstract":"Traumatic brain injury (TBI) is defined as structural damage or physiological disruption of brain function resulting from mechanisms such as direct impact, rapid acceleration or deceleration, penetrating injury, or exposure to blast waves. These biomechanical insults initiate a complex cascade of secondary injury processes, including neuronal cell death, neuroinflammation, oxidative stress, microglial activation, and blood-brain barrier dysfunction. These events contribute to the loss of homeostasis in both the central and peripheral nervous systems. Importantly, these pathophysiological changes may extend beyond the acute phase, often evolving into chronic conditions that can persist for years after the initial injury. In addition, TBI can cause fractures of the skull base and predispose to CSF leak and CSF fistula, which contribute to the contraction of bacteria. Surgical interventions, invasive devices, and prolonged immobilization are other factors that predispose patients to develop an infection secondary to TBI. Among the infections developed secondarily by patients with TBI are meningitis, pneumonia, and urinary tract infections, which can progress to Systemic Inflammatory Response Syndrome (SIRS) and sepsis. Furthermore, immunosuppression due to the lack of components of the cellular immune response, particularly neutrophils, helper T cells, regulatory T cells, and natural killer (NK) cells, demonstrates the pathophysiological heterogeneity of TBI, which can result in complications involving the central nervous system (CNS) and peripheral nervous system (PNS). Understanding how these secondary infections impact patient prognosis becomes necessary for more individualized therapies for each patient.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"235"},"PeriodicalIF":3.5,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144497493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ivermectin's neuroprotective effects decrease with prolonged use after cerebral ischemia/reperfusion. 脑缺血/再灌注后伊维菌素的神经保护作用随使用时间延长而降低。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-25 DOI: 10.1007/s11011-025-01657-z

Sevda Rezaei, Shabnam Babataheri, Hamid Soraya

{"title":"Ivermectin's neuroprotective effects decrease with prolonged use after cerebral ischemia/reperfusion.","authors":"Sevda Rezaei, Shabnam Babataheri, Hamid Soraya","doi":"10.1007/s11011-025-01657-z","DOIUrl":"10.1007/s11011-025-01657-z","url":null,"abstract":"Ivermectin (IVM), the recipient of the 2015 Nobel Prize, is an FDA-approved drug for a variety of parasitic diseases in animals and humans. However, the implications of this compound on neurological disorders remain inadequately elucidated. Recently, our research team has elucidated the neuroprotective properties of ivermectin administered in three doses following cerebral ischemia/reperfusion (IR). The objective of the current investigation is to ascertain whether ivermectin sustains its neuroprotective properties through prolonged administration in models of cerebral IR in rats, as well as to evaluate its impact on the formation of neutrophil extracellular traps (NETs). A rat model of transient global cerebral IR was induced by occluding both carotid arteries for 20 min. Ivermectin (2 mg/kg/day) was administered intraperitoneally one hour after the induction of cerebral ischemia for 7 consecutive days at 24-hour intervals. Then, the effects of ivermectin on brain infarct size, blood cell profile, bleeding time, memory and learning, balance and motor coordination, myeloperoxidase enzyme activity, and H3cit protein levels were investigated. The finding showed that the administration of ivermectin for 7 days did not improve memory and learning, blood parameters, or cerebral infarct size. However, it caused a 25.4% reduction in citrullinated histone protein level, decreased myeloperoxidase activity (P = 0.017), and improved balance and motor coordination (P = 0.017 and P = 0.024). In conclusion, our findings indicate that prolonged administration of ivermectin may diminish its neuroprotective effects and its effects can differ depending on the drug regimen.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"234"},"PeriodicalIF":3.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144485098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An analysis of the therapeutic efficacy and underlying mechanisms of combining lycopene with dental pulp stem cells to ameliorate alzheimer's disease in rats. 番茄红素联合牙髓干细胞治疗大鼠阿尔茨海默病的疗效及机制分析。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-24 DOI: 10.1007/s11011-025-01661-3

Zhiguo Xu, Yi Zhu, Lefeng Liu, Chao Liu, Zhongshan Zhang, Minghe Li, Linhua Yao, Feng Wang, Zhilong Dong, Shaorong Gao, Lan Kang, Lei Shi

引用次数: 0

Differential effects of industrial and ruminant trans fatty acids on appetitive memory. 工业反式脂肪酸和反刍动物反式脂肪酸对食欲记忆的不同影响。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-21 DOI: 10.1007/s11011-025-01656-0

J Alfredo Mendez, Mariana Dorantes-Gilardi

{"title":"Differential effects of industrial and ruminant trans fatty acids on appetitive memory.","authors":"J Alfredo Mendez, Mariana Dorantes-Gilardi","doi":"10.1007/s11011-025-01656-0","DOIUrl":"10.1007/s11011-025-01656-0","url":null,"abstract":"Trans-fatty acids (TFAs) are categorized into industrial TFAs (iTFAs) and ruminant TFAs (rTFAs). TFAs intakes over 48 mg/kg have been strongly associated with high risk of atherosclerosis and cardiovascular disease. However, some rTFAs have not been conclusively associated with coronary disease. Moreover, some health benefits have been suggested for rTFAs. Here, with the goal of contrasting the effects of iTFAs with rTFAs, we fed adult mice for 45 days with 168 mg/kg of trans-elaidic acid (TEA, an iTFA) or trans-vaccenic acid (TVA, an rTFA), and evaluated their serum lipid profile and their performance in an appetitive memory task. We found marked differential effects, while TEA showed strong atherogenic effects (p < 0.0001 for cholesterol, triglycerides, VLDL, LDL, and HDL versus control), TVA showed significant opposite effects than TEA (p < 0.0001 for cholesterol, triglycerides, LDL, and HDL; p = 0.0039 for VLDL). Furthermore, when these mice were trained to find a piece of feed in a slightly intricate eight-arm maze, TEA showed impairing effects on appetitive memory. Although TEA intake did not block appetitive memory, there was a clear delay in learning (p = 0.0353 versus control). Notably, TVA improved the learning performance of mice (p < 0.0001 versus control). Moreover, oleic acid, a cis isomer, showed similar effects than TVA in the appetitive learning task (p = 0.0004). Our results add to the hypothesis that intake of iTFAs have adverse effects whereas naturally occurring rTFAs could have some beneficial effects.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"232"},"PeriodicalIF":3.5,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tanshinone IIA inhibits neuronal ferroptosis and relieves cerebral ischemia‒reperfusion injury by regulating miR-449a/ACSL4. 丹参酮IIA通过调节miR-449a/ACSL4抑制神经元铁下垂，减轻脑缺血再灌注损伤。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-21 DOI: 10.1007/s11011-025-01660-4

Huimin Yu, Yili Li, Yuehong Yang, Yanjin Qian, Xia Gao, Xichan Wang, Ping Zhan, Dekun Tang, Mei Qin, Yan Qian

{"title":"Tanshinone IIA inhibits neuronal ferroptosis and relieves cerebral ischemia‒reperfusion injury by regulating miR-449a/ACSL4.","authors":"Huimin Yu, Yili Li, Yuehong Yang, Yanjin Qian, Xia Gao, Xichan Wang, Ping Zhan, Dekun Tang, Mei Qin, Yan Qian","doi":"10.1007/s11011-025-01660-4","DOIUrl":"10.1007/s11011-025-01660-4","url":null,"abstract":"Cerebral ischemia‒reperfusion injury (CI/RI) plays a significant role in the initiation of ischemic stroke. This study aimed to explore the influence of Tan (tanshinone) IIA in the treatment of neuronal ferroptosis induced by CI/RI, along with the associated molecular mechanisms. A CI/RI model was created by occluding the middle cerebral artery in rats (MCAO/R). A cellular CI/RI model was established with SH-SY5Y cells that were subjected to oxygen‒glucose deprivation followed by subsequent reperfusion (OGD/R). The optimal concentration for maintaining cell viability was evaluated through the CCK-8 assay. The expression levels of ferroptosis and oxidative stress-related genes in rat brain tissue and SH-SY5Y cells were determined, and the molecular mechanism by which Tan IIA regulates ferroptosis during CI/RI treatment was verified by bioinformatics analysis, RT‒qPCR, and dual-luciferase reporter assays. The results revealed that Tan IIA relieved CI/RI injury and inflammation by inhibiting ferroptosis in MCAO/R rat brain neurons. Our experimental results demonstrated that Tan IIA suppressed the progression of OGD/R and alleviated inflammation in SH-SY5Y cells. Ferroptosis affected the concentrations of Fe2+, ROS, and MDA in the CI/RI model while simultaneously increasing the expression of miR-449a. In terms of the molecular mechanism, Tan IIA inhibited OGD/R-induced neural ferroptosis, and this mechanism of action may involve Tan IIA promoting the downregulation of ACSL4 expression by targeting miR-449a within cells, thereby inhibiting ferroptosis in cells induced by OGD/R. Our research results indicate that Tan IIA relieved CI/RI injury and inflammation by alleviating neuronal ferroptosis, and this regulatory effect may be achieved through the miR-449a/ACSL4 molecular axis.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"231"},"PeriodicalIF":3.5,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolomic analysis of blood spots in a Chinese cohort with autism spectrum disorders: a pilot study. 中国自闭症谱系障碍患者血斑代谢组学分析：一项初步研究。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-20 DOI: 10.1007/s11011-025-01635-5

Hui Wang, Li Ding, Zheng-Huan Mao, Yu Du, Qing-Mei Han, Jia-Yu Xu, Fei-Fei Peng, Hai-Feng Li, Chao-Chun Zou

{"title":"Metabolomic analysis of blood spots in a Chinese cohort with autism spectrum disorders: a pilot study.","authors":"Hui Wang, Li Ding, Zheng-Huan Mao, Yu Du, Qing-Mei Han, Jia-Yu Xu, Fei-Fei Peng, Hai-Feng Li, Chao-Chun Zou","doi":"10.1007/s11011-025-01635-5","DOIUrl":"10.1007/s11011-025-01635-5","url":null,"abstract":"Autism spectrum disorder (ASD) is a neurodevelopmental disorder with a strong genetic component that is becoming increasingly prevalent. The identification of plasma molecular biomarkers may provide potential insights into ASD and aid in early diagnosis. In this study, we characterized the metabolomic profiles of ASD children using blood spot samples collected at the Children's Hospital of Zhejiang University School of Medicine from children with ASD (n = 43) and typically developing (TD) children (n = 43). Our results highlight differences between children with ASD and TD controls. We identified possibly associations between ASD and a variety of metabolites, including carnosine (Car), glutaric acid, histidine (His), succinic acid, tryptophan, glutamine (Gln), asparagine, guanidinoacetic acid, sarcosine, kynurenine, glutamic acid (Glu) and cysteine (Cys). Metabolic pathway analysis demonstrated a possible imbalance in the amino acid metabolism of Glu/Gln, Car/His in ASD children. These findings may provide new insights into the molecular mechanisms that influence ASD risk and have possibility for the discovery of biomarkers.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"230"},"PeriodicalIF":3.5,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cola acuminata extract's inhibition of NLRP3 inflammasome in THP-1 cells as a potential treatment option for Parkinson's disease. 可乐提取物抑制THP-1细胞中NLRP3炎性体作为帕金森病的潜在治疗选择

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-19 DOI: 10.1007/s11011-025-01628-4

Brice Ayissi Owona, Viviane Ndam Ngoungoure, Jordas Tchana Tchamba, Frederic Nico Njayou, Paul Fewou Moundipa

{"title":"Cola acuminata extract's inhibition of NLRP3 inflammasome in THP-1 cells as a potential treatment option for Parkinson's disease.","authors":"Brice Ayissi Owona, Viviane Ndam Ngoungoure, Jordas Tchana Tchamba, Frederic Nico Njayou, Paul Fewou Moundipa","doi":"10.1007/s11011-025-01628-4","DOIUrl":"10.1007/s11011-025-01628-4","url":null,"abstract":"Neuroinflammation has been described as one of the multiple clinical manifestations of Parkinson's and Alzheimer's diseases (PD and AD). Moreover, it was reported that amyloid-β deposition is associated with cognitive decline in PD. Here, Cola acuminata (CA) extract was used to inhibit NLRP3 inflammasome in THP-1 macrophages in vitro. CA showed significant anti-inflammatory effect by inhibiting nitric oxide (NO) release from cells after stimulation with LPS and Nigericin. Phagocytosis of amyloid-β by THP-1 cells showed that at 100 µg/ml, CA increases phagocytic activity of macrophages in vitro. Moreover, activation of NLRP3 inflammasome and subsequent treatment with CA showed a reduction of IL1-β and IL-18 cytokines release in ELISA assay. Furthermore, NLRP3, caspase-1, IL1-β and NF-kB expressions were significantly inhibited at the gene and protein levels as shown by RTqPCR and western blot assays respectively. Interestingly, colocalization analysis of activated inflammasome confirmed our results suggesting that CA disaggregates inflammasome assembly. Mass spectrometry analysis of CA has identified epicatechin, catechin, chlorogenic acid, quercetin and stigmasterol known as inflammasome inhibitors among the extract chemical constituents. Together, our results indicate that CA can inhibit inflammasome activation in macrophage, thereby opening future perspectives for PD treatment.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"229"},"PeriodicalIF":3.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144326274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rice bran extract attenuates cognitive impairment by enhancing pancreatic β-cell insulin secretion in STZ-induced diabetic rats targeting the PPARγ/PDX1 pathway. 米糠提取物通过增强stz诱导的糖尿病大鼠胰腺β细胞胰岛素分泌，靶向PPARγ/PDX1通路，减轻认知障碍。

IF 3.5 3区医学

Metabolic brain disease Pub Date : 2025-06-19 DOI: 10.1007/s11011-025-01639-1

Madonna Magdy Youssef, Mohammed Farrag El-Yamany, Reham Mahmoud Abdel-Kader, Ola Ahmed Heikal

{"title":"Rice bran extract attenuates cognitive impairment by enhancing pancreatic β-cell insulin secretion in STZ-induced diabetic rats targeting the PPARγ/PDX1 pathway.","authors":"Madonna Magdy Youssef, Mohammed Farrag El-Yamany, Reham Mahmoud Abdel-Kader, Ola Ahmed Heikal","doi":"10.1007/s11011-025-01639-1","DOIUrl":"10.1007/s11011-025-01639-1","url":null,"abstract":"Type I diabetes (T1D), also known as juvenile diabetes, is an autoimmune disease that causes gradual destruction of pancreatic cells and leads to intellectual disability, neuropathy, cognitive impairment, and impaired learning ability in children. Despite standard treatment with synthetic human insulin, T1D patients can maintain up to 40% of their insulin-producing islets. PPARγ receptor activation research that aims to restore β-cell biology could help reverse the loss of pancreatic mass that comes with getting older and improve β-cell function. Egyptian RB ethanol extract (RBE), previously reported with PPARγ agonist activity, showed an increase in insulin secretion both in vivo and in INS-1 cells. The exact antidiabetic RBE mechanism is still unclear. The present study aims to investigate the molecular RBE mechanism in glucose-stimulating insulin secretion and restoration of β cell function. A diabetic rat streptozotocin (STZ) model was used; five groups were designed. The STZ-diabetic rats were treated with RBE daily for 21 days compared to an insulin-treated group. Biochemical parameters and quantitative RT-PCR of β-cell genes related to the PPAR/PDX1 signaling pathway were performed, and the influence on cognitive ability was confirmed by behavioral testing (Y-maze and NOR) and histological examination. The RBE-treated group reversed blood glucose, Glut2, Ca2 +, and insulin levels in diabetic rats, with pancreatic insulin levels significantly increasing compared to the insulin group. With the exception of PDX1, RBE boosted PPARγ, SERCA, and PrKC gene expression. RBE also restored cognitive functions. This study suggests that RBE may enhance memory and cognition by increasing peripheral insulin secretion through PPARγ regulator activity.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 6","pages":"228"},"PeriodicalIF":3.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144326275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0