Resveratrol attenuates arsenic-induced cognitive deficits via modulation of Estrogen-NMDAR-BDNF signalling pathway in female mouse hippocampus

Mehta, Kamakshi; Pandey, Kamlesh Kumar; Kaur, Baljinder; Dhar, Pushpa; Kaler, Saroj

doi:10.1007/s00213-021-05871-2

Cited by 14 publications

(10 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Considering the high number of people worldwide consuming water contaminated with arsenic as well as its neurotoxic properties, scientists decided to utilize arsenic to induce CNS dysfunctions in rodents and investigate whether supplementation with resveratrol could reverse the observed changes (Mehta et al, 2021; Taheri Zadeh et al, 2021). Arsenic administered for prolonged periods caused cognitive impairments and anxiety‐like behaviors in animals.…”

Section: Stilbenes In Neuropsychiatric and Neurological Disordersmentioning

confidence: 99%

“…Arsenic administered for prolonged periods caused cognitive impairments and anxiety‐like behaviors in animals. Mehta et al (2021) discovered that resveratrol, at the dose of 40 mg/kg, increased the time female Swiss albino mice spent in the open field and open arms compared to arsenic‐alone treated group, hence, suggesting that the supplementation with this plant‐based antioxidant has potential anxiolytic‐like properties and reduces inorganic arsenic ( iAs )‐induced neurotoxicity. Additionally, scientists observed that resveratrol decreased iAs levels in both brain tissue and serum (Mehta et al, 2021).…”

Section: Stilbenes In Neuropsychiatric and Neurological Disordersmentioning

confidence: 99%

“…utilize arsenic to induce CNS dysfunctions in rodents and investigate whether supplementation with resveratrol could reverse the observed changes(Mehta et al, 2021;Taheri Zadeh et al, 2021). Arsenic administered for prolonged periods caused cognitive impairments and anxiety-like behaviors in animals.Mehta et al …”

mentioning

confidence: 99%

See 2 more Smart Citations

Therapeutic potential of stilbenes in neuropsychiatric and neurological disorders: A comprehensive review of preclinical and clinical evidence

Socała,

Żmudzka,

Lustyk

et al. 2024

Phytotherapy Research

View full text Add to dashboard Cite

Neuropsychiatric disorders are anticipated to be a leading health concern in the near future, emphasizing an outstanding need for the development of new effective therapeutics to treat them. Stilbenes, with resveratrol attracting the most attention, are an example of multi‐target compounds with promising therapeutic potential for a broad array of neuropsychiatric and neurological conditions. This review is a comprehensive summary of the current state of research on stilbenes in several neuropsychiatric and neurological disorders such as depression, anxiety, schizophrenia, autism spectrum disorders, epilepsy, traumatic brain injury, and neurodegenerative disorders. We describe and discuss the results of both in vitro and in vivo studies. The majority of studies concentrate on resveratrol, with limited findings exploring other stilbenes such as pterostilbene, piceatannol, polydatin, tetrahydroxystilbene glucoside, or synthetic resveratrol derivatives. Overall, although extensive preclinical studies show the potential benefits of stilbenes in various central nervous system disorders, clinical evidence on their therapeutic efficacy is largely missing.

show abstract

Section: Stilbenes In Neuropsychiatric and Neurological Disordersmentioning

confidence: 99%

Section: Stilbenes In Neuropsychiatric and Neurological Disordersmentioning

confidence: 99%

See 1 more Smart Citation

Therapeutic potential of stilbenes in neuropsychiatric and neurological disorders: A comprehensive review of preclinical and clinical evidence

Socała,

Żmudzka,

Lustyk

et al. 2024

Phytotherapy Research

View full text Add to dashboard Cite

show abstract

“…Natural estrogens mainly include estrone (E1), estradiol (E2), and estriol (E3). Among them, E2 is the most abundant estrogen with the strongest activity, which has significant neuroprotective effects on different kinds of brain injury [ 42 ]. Studies have shown that E2 plays a neuroprotective role in ischemic neuron injury by inhibiting the expression and function of acid-sensitive ion channel proteins in an ischemic stroke model [ 43 ].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Mechanism of Icariin on Hypoxic Ischemic Brain Damage in Neonatal Mice

Wang

Yang

Zhou

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Objective. Our previous results showed that icariin (ICA) could inhibit apoptosis and provide neuroprotection against hypoxic-ischemic brain damage (HIBD) in neonatal mice, but the specific mechanism of its neuroprotective effect remains unknown. This study aims at exploring whether ICA plays a neuroprotective role in apoptosis inhibition by regulating autophagy through the estrogen receptor α (ERα)/estrogen receptor β (ERβ) pathway in neonatal mice with HIBD. Methods. A neonatal mouse model of HIBD was constructed in vivo, and an oxygen and glucose deprivation (OGD) model in HT22 cells from the hippocampal neuronal system was constructed in vitro. The effects of ICA pretreatment on autophagy and the expression of ERα and ERβ were detected in vitro and in vivo, respectively. ICA pretreatment was also supplemented with the autophagy inhibitor 3-methyladenine (3-MA), ERα inhibitor methylpiperidino pyrazole (MPP), and ERβ inhibitor 4-(2-phenyl-5,7-bis (trifluoromethyl) pyrazolo [1,5-a] pyramidin-3-yl) phenol (PHTPP) to further detect whether ICA pretreatment can activate the ERα/ERβ pathway to promote autophagy and reduce HIBD-induced apoptosis to play a neuroprotective role against HIBD in neonatal mice. Results. ICA pretreatment significantly promoted autophagy in HIBD mice. Treatment with 3-MA significantly inhibited the increase in autophagy induced by ICA pretreatment, reversed the neuroprotective effect of ICA pretreatment, and promoted apoptosis. Moreover, ICA pretreatment significantly increased the expression levels of the ERα and ERβ proteins in HIBD newborn mice. Both MPP and PHTPP administration significantly inhibited the expression levels of the ERα and ERβ proteins activated by ICA pretreatment, reversed the neuroprotective effects of ICA pretreatment, inhibited the increase in autophagy induced by ICA pretreatment, and promoted apoptosis. Conclusion. ICA pretreatment may promote autophagy by activating the ERα and ERβ pathways, thus reducing the apoptosis induced by HIBD and exerting a neuroprotective effect on neonatal mice with HIBD.

show abstract

“…Natural estrogens mainly include estrone (E1), estradiol (E2), and estriol (E3). Among them, E2 is the estrogen with the most content and the strongest activity, which has signi cant neuroprotective effects on different kinds of brain injury [57]. Studies have shown that E2 plays a neuroprotective role in ischemic neuron injury by inhibiting the expression and function of acid-sensitive ion channel proteins in the ischemic stroke model [58].…”

mentioning

confidence: 99%

Neuroprotective mechanism of icariin on hypoxic- ischemic brain damage in neonatal mice

Wang

Yang

Zhou

et al. 2022

Preprint

View full text Add to dashboard Cite

Objective: Hypoxic-ischemic brain damage (HIBD) is one of the leading causes of permanent neurological dysfunction and acute death in infants and young children. As the only effective treatment for neonatal HIBD, therapeutic hypothermia (TH) can only moderately improve the prognosis. Previous evidence has shown that icariin (ICA) can inhibit apoptosis and exert a neuroprotective effect on neonatal mouse HIBD, but the specific mechanism remains unknown. This study aimed to explore whether ICA played a neuroprotective role in inhibiting apoptosis by regulating autophagy through the estrogen receptor α (ERα) and estrogen receptor β (ERβ) pathways in neonatal mice with HIBD.Method: In vivo experiments, the HIBD model of neonatal mice were constructed according to the modified Rice-Vannucci method. The effects of ICA on the expression levels of autophagy-related proteins as well as ERα and ERβ proteins were detected. At the same time as ICA pretreatment, HIBD newborn mice were injected with the autophagy inhibitor 3-MA into the lateral ventricle to test whether ICA pretreatment might exert the neuroprotective effect of HIBD on newborn mice by promoting autophagy and inhibiting HIBD-induced apoptosis. At the same time as ICA pretreatment, HIBD newborn mice were injected with ERα inhibitor MPP or ERβ inhibitor PHTPP into the lateral ventricle, to further test whether ICA might promote autophagy and inhibit HIBD-induced apoptosis by activating ERα or ERβ pathways, thereby exerting a neuroprotective effect on HIBD in newborn mice. The cerebral infarct volume and the degree of brain injury in the mice were evaluated by TTC staining and brain water content determination. Body weight measurements and neurobehavioral tests were carried out to assess neurological recovery after HIBD in neonatal mice; The expressions of ERα, ERβ, autophagy and apoptosis-related proteins were detected by tissue immunofluorescence and western blot, and the level of apoptosis was further detected by TUNEL and FJC staining. A caspase-3 activity detection kit was used to detect the relative activity level of caspase-3. The glucose and oxygen deprivation (OGD) model of HT22 cells in the mouse hippocampal neuron system was constructed and experimented in vitro.Result: ICA pretreatment significantly promoted the autophagy level of HIBD mice. Treatment with 3-MA significantly inhibited the increase of autophagy induced by ICA pretreatment, reversed the neuroprotective effect of ICA pretreatment, and promoted apoptosis. ICA pretreatment significantly increased the expression levels of ERα and ERβ proteins in HIBD newborn mice. The MPP and PHTPP treatments significantly inhibited the expression levels of ERα and ERβ proteins activated by ICA pretreatment, reversed the neuroprotective effects of ICA pretreatment, inhibited the increase in autophagy induced by ICA pretreatment, and promoted apoptosis.Conclusion: ICA pretreatment may promote autophagy by activating the ERα and ERβ pathway, and thus reduce the apoptosis induced by HIBD, then exert a neuroprotective effect on neonatal mice with HIBD.

show abstract

Resveratrol attenuates arsenic-induced cognitive deficits via modulation of Estrogen-NMDAR-BDNF signalling pathway in female mouse hippocampus

Cited by 14 publications

References 92 publications

Therapeutic potential of stilbenes in neuropsychiatric and neurological disorders: A comprehensive review of preclinical and clinical evidence

Therapeutic potential of stilbenes in neuropsychiatric and neurological disorders: A comprehensive review of preclinical and clinical evidence

Neuroprotective Mechanism of Icariin on Hypoxic Ischemic Brain Damage in Neonatal Mice

Neuroprotective mechanism of icariin on hypoxic- ischemic brain damage in neonatal mice

Contact Info

Product

Resources

About