Ursolic Acid Protects Neurons in Temporal Lobe Epilepsy and Cognitive Impairment by Repressing Inflammation and Oxidation

Liu, Kunmei; Huang, Yue; Wan, Pan-pan; Lu, Yunhua; Zhou, Ning; Li, Juanjuan; Yu, Chunyang; Chou, Jinjiang; Zhang, Lian-xiang; Zhang, Chun; Qiang, Yuan-yuan; Zhang, Rui; Guo, Le

doi:10.3389/fphar.2022.877898

Cited by 11 publications

(12 citation statements)

References 49 publications

(54 reference statements)

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“…Interestingly, UA exhibit significant restoration of the expression levels of these markers in comparison to RA and donepezil (Mirza et al, 2021). It also enhanced neurogenesis and repressed inflammation in temporal lobe epilepsy and cerebral ischemia models Liu et al, 2022). Its role in neurite outgrowth and neuronal survival mediated by nerve growth factor has also been reported (Theis et al, 2018).…”

Section: Discussionmentioning

confidence: 88%

Ursolic acid and rosmarinic acid ameliorate alterations in hippocampal neurogenesis and social memory induced by amyloid beta in mouse model of Alzheimer’s disease

Mirza

Zahid

2022

Front. Pharmacol.

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Alzheimer’s disease (AD) is a multifaceted neurodegenerative disorder characterized by substantial neuronal damage which manifests in the form of deficits in memory and cognition. In spite of the debilitating nature of Alzheimer’s disease (AD), a dearth of treatment strategies calls for the need to develop therapeutic agents that stimulate neurogenesis and alleviate the associated cognitive deficits. The present study investigates the therapeutic potential of two major phytochemicals, rosmarinic acid (RA) and ursolic acid (UA) in an amyloid beta1–42 (Aβ1–42)-induced model of AD. UA, a natural pentacyclic triterpenoid and RA, a phenolic ester are major bioactive constituents of Rosmarinus officinalis, which is a medicinal herb belonging to family Lamiaceae and exhibiting significant biological properties including neuroprotection. Donepezil, a second generation cholinesterase inhibitor approved for the treatment of mild, moderate and severe Alzheimer’s disease (AD) is used as control. Out of eight groups of male BALB/c mice, stereotaxic surgery was performed on four groups (n = 6 each) to introduce Aβ1–42 in the hippocampus followed by treatment with vehicle (phosphate-buffered saline (PBS)), donepezil, UA or RA. The other four groups were given vehicle, donepezil, UA and RA only. Behavior analysis for social interaction was performed which constitutes the social affiliation and the social novelty preference test. Presence of Aβ plaques and expression of neurogenesis markers i.e., doublecortin (DCX) and Ki-67 were also assessed. Results revealed the neuroprotective effect of UA and RA observed through substantial reduction in Aβ plaques as compared to the Aβ1-42- and donepezil-treated groups. The neuronal density was also restored as evident via DCX and Ki-67 immunoreactivity in Aβ1–42 + RA and Aβ1–42+UA-treated groups in comparison to Aβ1–42-treated and Aβ1–42+donepezil-treated groups. The social affiliation was reestablished in the Aβ1–42 administered groups treated with UA and RA. Molecular docking studies further validated the comparable binding of UA and RA with Ki-67 and DCX to that of donepezil. Our findings suggest that UA and RA are potential neuroprotective compounds that reverses the histological hallmarks of AD and ameliorate impaired social memory and hippocampal neurogenesis.

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Section: Discussionmentioning

confidence: 88%

Ursolic acid and rosmarinic acid ameliorate alterations in hippocampal neurogenesis and social memory induced by amyloid beta in mouse model of Alzheimer’s disease

Mirza

Zahid

2022

Front. Pharmacol.

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“…SE causes hippocampal damage by inducing inflammation, and hippocampal damage eventually leads to chronic TLE. Therefore, epilepsy-induced neuronal damage can be ameliorated through anti-inflammatory effects ( 22 , 43 – 45 ). Through the continuous study of the TLE mechanism, we can find the target of TLE treatment.…”

Section: Discussionmentioning

confidence: 99%

Progress in TLE treatment from 2003 to 2023: scientific measurement and visual analysis based on CiteSpace

Cao,

Guo,

Cao

et al. 2023

Front. Neurol.

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ObjectiveTemporal lobe epilepsy (TLE) is the most common cause of drug-resistant epilepsy and can be treated surgically to control seizures. In this study, we analyzed the relevant research literature in the field of temporal lobe epilepsy (TLE) treatment to understand the background, hotspots, and trends in TLE treatment research.MethodsWe discussed the trend, frontier, and hotspot of scientific output in TLE treatment research in the world in the last 20 years by searching the core collection of the Web of Science database. Excel and CiteSpace software were used to analyze the basic data of the literature.ResultWe identified a total of 2,051 publications on TLE treatment from 75 countries between 2003 and 2023. We found that the publication rate was generally increasing. The United States was the most publishing country; among the research institutions on TLE treatment, the University of California system published the most relevant literature and collaborated the most with other institutions. The co-citation of literature, keyword co-occurrence, and its clustering analysis showed that the early studies focused on open surgical treatment, mainly by lobectomy. In recent years, the attention given to stereotactic, microsurgery, and other surgical techniques has gradually increased, and the burst analysis indicated that new research hotspots may appear in the future in the areas of improved surgical procedures and mechanism research.

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“…A 2A R Expression in the Rat Hippocampus Some studies have shown that damage to hippocampal neurons can be accompanied by hippocampal inflammation [46][47][48]. TNF-α can induce nerve injury by mediating neuroinflammation and promoting T cells to produce various inflammatory factors [49].…”

Section: Cy Exposure Can Cause Abnormal Changes In the Inflammatory R...mentioning

confidence: 99%

Effects of Cyfluthrin Exposure on Neurobehaviour, Hippocampal Tissue and Synaptic Plasticity in Wistar Rats

Xie,

Zhao,

et al. 2023

Toxics

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This experiment was conducted to study the effects of Cyfluthrin (Cy) exposure on neurobehaviour, hippocampal tissue and synaptic plasticity in Wistar rats. First, it was found that high-dose Cy exposure could cause nerve injury, resulting in symptoms such as deficits in learning and memory ability, spatial exploration and autonomic motor function. Moreover, it was found that medium- and high-dose Cy exposure could cause an abnormal release of the neurotransmitter Glu. Second, brain tissue pathology showed that the middle and high doses of Cy caused tissue deformation, reduced the number of hippocampal puramidal cells, caused a disorder of these cells, decreased the number of Nissl bodies, and caused pyknosis of the hippocampal cell nuclear membrane and serious damage to organelles, indicating that exposure to these doses of Cy may cause hippocampal tissue damage in rats. Third, as the exposure dose increased, morphological changes in hippocampal synapses, including blurred synaptic spaces, a decreased number of synaptic vesicles and a decreased number of synapses, became more obvious. Moreover, the expression levels of the key synaptic proteins PSD-95 and SYP also decreased in a dose-dependent manner, indicating obvious synaptic damage. Finally, the study found that medium and high doses of Cy could upregulate the expression of A2AR in the hippocampus and that the expression levels of inflammatory factors and apoptosis-related proteins increased in a dose-dependent manner. Moreover, the expression of A2AR mRNA was correlated with neurobehavioural indicators and the levels of inflammatory factors, synaptic plasticity-related factors and apoptosis-related factors, suggesting that Cy may cause nerve damage in rats and that this effect is closely related to A2AR.

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Ursolic Acid Protects Neurons in Temporal Lobe Epilepsy and Cognitive Impairment by Repressing Inflammation and Oxidation

Cited by 11 publications

References 49 publications

Ursolic acid and rosmarinic acid ameliorate alterations in hippocampal neurogenesis and social memory induced by amyloid beta in mouse model of Alzheimer’s disease

Ursolic acid and rosmarinic acid ameliorate alterations in hippocampal neurogenesis and social memory induced by amyloid beta in mouse model of Alzheimer’s disease

Progress in TLE treatment from 2003 to 2023: scientific measurement and visual analysis based on CiteSpace

Effects of Cyfluthrin Exposure on Neurobehaviour, Hippocampal Tissue and Synaptic Plasticity in Wistar Rats

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