Lacidipine Prevents Scopolamine-Induced Memory Impairment by Reducing Brain Oxido-nitrosative Stress in Mice

Khurana, Kunal; Kumar, Manish; Bansal, Nitin

doi:10.1007/s12640-021-00346-w

Cited by 14 publications

(15 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, AChE overexpression is a reliable marker of aging, inflammatory states, and several diseases, such as hypertension, glaucoma, dementia, and anemia [51,53]. Additionally, scopolamine (i.e., a nonselective anticholinergic medication) was found to increase AChE activity in several different experimental models [54,55], though the role of anticholinergic-induced AChE overexpression in the pathophysiology of anemia is still to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

The Interplay between Anticholinergic Burden and Anemia in Relation to 1-Year Mortality among Older Patients Discharged from Acute Care Hospitals

Corsonello

Soraci

Corica

et al. 2021

JCM

View full text Add to dashboard Cite

Anticholinergic burden (ACB) and anemia were found associated with an increased risk of death among older patients. Additionally, anticholinergic medications may contribute to the development of anemia. Therefore, we aimed at investigating the prognostic interplay of ACB and anemia among older patients discharged from hospital. Our series consisted of 783 patients enrolled in a multicenter observational study. The outcome of the study was 1 year mortality. ACB was assessed by an Anticholinergic Cognitive Burden score. Anemia was defined as hemoglobin < 13 g/dL in men and <12 g/dL in women. The association between study variables and mortality was investigated by Cox regression analysis. After adjusting for several potential confounders, ACB score = 2 or more was significantly associated with the outcome in anemic patients (HR = 1.93, 95%CI = 1.13–3.40), but not non anemic patients (HR = 1.51, 95%CI = 0.65–3.48). An additive prognostic interaction between ACB and anemia was observed (p = 0.02). Anemia may represent a relevant effect modifier in the association between ACB and mortality.

show abstract

Section: Discussionmentioning

confidence: 99%

The Interplay between Anticholinergic Burden and Anemia in Relation to 1-Year Mortality among Older Patients Discharged from Acute Care Hospitals

Corsonello

Soraci

Corica

et al. 2021

JCM

View full text Add to dashboard Cite

show abstract

“…routes. This drug disrupts the cholinergic tracts in areas responsible for cognition and memory [16] , [17] , [18] .…”

Section: Methods Detailsmentioning

confidence: 99%

“… 0.3-0.5mg/kg (i.p.) 72µg/0.5µl (i.c.v) [16] , [17] , [18] 4. AF64A induced memory deficits Male Wistar-Imamichi rats, aged 7-8weeks.…”

Section: Introductionmentioning

confidence: 99%

Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease

2022

View full text Add to dashboard Cite

“…By contrast to neuroprotective effects of P/Q-type and N-type calcium channel blockers, there is a gap for L-type calcium channels blockers in relation to glutamate excitotoxicity (Vallazza-Deschamps et al, 2005;Wheeler et al, 1996). Although there are studies demonstrating the neuroprotective effects of lacidipine and amlodipine which are dihydropyridine calcium channel blockers, evidence supporting their roles as a neuroprotectant factor in glutamate excitotoxicity is almost not available (Choi et al, 2014;Khurana et al, 2021). Both lacidipine and amlodipine block L-channels, but their selectivity is different.…”

Section: Introductionmentioning

confidence: 99%

The Difference Between The Response To Glutamate Excitotoxicity and The Role Of Ca2+ Channel Blockers in Cortical Neuron and SH-SY5Y Cells Cultures

Çiçek

Taghizadehghalehjoughi

Hacımüftüoğlu³

et al. 2022

Journal of Anatolian Environmental and Animal Sciences

View full text Add to dashboard Cite

Cortical neuron and SH-SY5Y cells are widely used in glutamate excitotoxicity studies, but it is unclear which one better reflects this model. Generally, glutamate induces toxicity conditions by leading to L and L/N-Ca 2+ channels activation and cell death via lethal Ca 2+ influx. To evaluate this hypothesis, the effects of L and L/N-Ca 2+ channel blockers, lacidipine, and amlodipine under excitotoxic conditions were evaluated. At the same time, in this study, we aimed to determine that these two cell lines better reflect this model. To induce excitotoxicity, cortical neuron and SH-SY5Y cells were incubated with glutamate 10 -5 mM. After 30 min incubation with glutamate, agents of different concentrations (1, 2, and 4 µg lacidipine and 20, 50, and 100 µM amlodipine) were applied to these cells. Possible neuroprotective roles of lacidipine and amlodipine were investigated through cell viability, oxidative stress, and apoptotic alterations. Our results showed that SH-SY5Y cells are the more ideal cell line for oxidative stress-mediated glutamate toxicity. Although 4 µg lacidipine and 100 µM amlodipine have important neuroprotective roles in these cells, the most protective effect was also detected in SH-SY5Y cells at 100 µM amlodipine concentration. The highest viability rate on cell lines was found at 88.8 % in SH-SY5Y cells treated with 100 μM amlodipine. Results from the TAC, TOS, LDH assays, and flow cytometry analysis were correlated to our MTT results. Taken together, our results indicate that SH-SY5Y cells are more effective at reflecting glutamate-induced excitotoxicity and 100μM amlodipine has a more protective effect in treating this toxicity.

show abstract

Lacidipine Prevents Scopolamine-Induced Memory Impairment by Reducing Brain Oxido-nitrosative Stress in Mice

Cited by 14 publications

References 81 publications

The Interplay between Anticholinergic Burden and Anemia in Relation to 1-Year Mortality among Older Patients Discharged from Acute Care Hospitals

The Interplay between Anticholinergic Burden and Anemia in Relation to 1-Year Mortality among Older Patients Discharged from Acute Care Hospitals

Experimentally induced animal models for cognitive dysfunction and Alzheimer's disease

The Difference Between The Response To Glutamate Excitotoxicity and The Role Of Ca2+ Channel Blockers in Cortical Neuron and SH-SY5Y Cells Cultures

Contact Info

Product

Resources

About