Protective effects of nimodipine on cerebrovascular function in chronic alcoholic encephalopathy

Li, Hui; Yang, Xue; Wei, Shi; Ma, Zhao; Feng, Guangshen; Wang, Qinzhou; Shen, Li; Xie, Chunli

doi:10.3892/ijmm.2013.1540

Cited by 9 publications

(9 citation statements)

References 29 publications

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“…18 Meanwhile, Li et al found that TET could protect rat from alcoholic-induced chronic alcoholic encephalopathy. 7 These results were consistent with our finding, and confirmed TET may serve as a neuroprotective role in BUP-treated SH-SY5Y cells.…”

Section: Discussionsupporting

confidence: 92%

“…Tetramethylpyrazine (TET) is an alkaloid that originally extracted from a traditional Chinese herbal medicine Ligusticum chuanxiong. 7,8 TET has been used as an effective compound to remedy patients with kidney, heart and brain diseases. [9][10][11] In addition, TET also has been reported to provide neuroprotective effect against ischemic brain damage in rats.…”

Section: Introductionmentioning

confidence: 99%

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<p>Tetramethylpyrazine attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells through regulating apoptosis, autophagy and oxidative damage</p>

Wang¹,

Xia²,

Qiao³

et al. 2019

DDDT

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Background: Bupivacaine (BUP) acts as a local anesthetic, which is extensively used for clinical patients but could generate neurotoxicity in neurons. Tetramethylpyrazine (TET) exhibits strong neuron protective effects against neurotoxicity. Hence, we investigate the effect of TET on BUP-induced neurotoxicity in SH-SY5Y cells. Methods: CCK-8 assay was used to detect cell proliferation in SH-SY5Y cells. In addition, Western blotting was used to examine Bax, Bcl-2, active caspase 3, LC3II, Beclin 1 and p-62 protein levels in cells. Moreover, ELISA assay was used to detect the levels of total glutathione (GS), superoxide dismutase (SOD) and malondialdehyde (MDA) in cells. Results: In this study, we found that TET attenuated the neurotoxicity of BUP on SH-SY5Y cells. Meanwhile, TET alleviated BUP-induced apoptosis in SH-SY5Y cell via decreasing the expressions of active caspase-3 and Bax and increasing the expression of Bcl-2. In addition, monodansylcadaverine staining assay and Western blotting results confirmed that TET induced autophagy in SH-SY5Y cells via increasing the LC3II/I and Beclin 1 levels. Furthermore, TET attenuated BUP-induced oxidative damage in SH-SY5Y cells via upregulation of the levels of total GS and SOD and downregulation of the level of MDA. Interesting, the protective effects of TET against BUP-induced neurotoxicity in SH-SY5Y cells were reversed by autophagy inhibitor 3-methyladenine (3MA). Conclusion: These data indicated that TET may play a neuroprotective role via inhibiting apoptosis and inducing autophagy in SH-SY5Y cells. Therefore, TET may be a potential agent for the treatment of human neurotoxicity induced by BUP.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

<p>Tetramethylpyrazine attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells through regulating apoptosis, autophagy and oxidative damage</p>

Wang¹,

Xia²,

Qiao³

et al. 2019

DDDT

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“…It can expand the cerebral blood vessels, improve the cerebral circulation, and protect the brain. [6,7] Studies have shown that nimodipine could improve cognition in adult mice by reducing neuronal damage [8] and our previous research found pretreatment with nimodipine can prevent postoperative cognitive dysfunction (POCD) on aged rats by reducing hippocampal apoptosis rate. [9] However, its clinical effect remains to be discussed.…”

Section: Introductionmentioning

confidence: 99%

Effects of nimodipine on postoperative delirium in elderly under general anesthesia

Zhou

Yin

et al. 2017

Medicine

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Nimodipine is a clinical commonly used calcium antagonistscan lowering the apoptosis rate of hippocampal neuron to reduce the incidence of postoperative cognitive dysfunction (POCD). This study was designed to evaluate the effects of nimodipine on postoperative delirium in elderly under general anesthesia.Sixty patients shceduced spine surgery under general anesthesia were randomly assigned into 2 groups using a random number table: control group (Group C) and nimodipine group (Group N). In Group N, nimodipine 7.5 μg/(kg × h) was injected continually 30 minutes before anesthesia induction, while the equal volume of normal saline was given in Group C. At 0 minute before injection, 0 minute after tracheal intubation, 1 hour after skin incision and surgery completed (T1–4), blood samples were taken from the radial artery and jugular bulb for blood gas analysis. Cerebral oxygen metabolism-related indicators were calculated at the same time. Concentration of S100β and glial fibrillary acidic protein (GFAP) were tested by ELISA. The incidence of postoperative delirium within 7 days after surgery was recorded.Cerebral oxygen metabolism-related indicators fluctuationed in the normal range in 2 groups at different time points and the difference were not statistically significant. Compared with Group C, S100β and GFAP decreased and incidence of postoperative delirium reduced at T3–4 in Group N, the difference was statistically significant (P<.05).The present study suggests that nimodipine can reduce the development of postoperative delirium in elderly patients under general anesthesia, the reduction of brain injury and improvement of cerebral oxygen metabolism may be involved in the mechanism.

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“…Administration of a calcium antagonist nimodipine may partly inhibit the apoptosis of neurons in the hippocampus and improve cognitive function following WBRT. Previous studies on cerebral ischemia, brain injury, chronic alcoholic encephalopathy, subarachnoid hemorrhage or cerebral hemorrhage demonstrated that calcium antagonists may exert a protective effect on brain function (12,(35)(36)(37)(38). The expression levels of calcium-associated genes decreased following cerebral ischemia, leading to inhibition of L-type calcium channels, which in turn may induce post-ischemic neuronal death.…”

Section: Discussionmentioning

confidence: 99%

Delayed cognitive deficits can be alleviated by calcium antagonist nimodipine by downregulation of apoptosis following whole brain radiotherapy

Tong

Zhang

et al. 2018

Oncol Lett

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Radiation therapy is important for the comprehensive treatment of intracranial tumors. However, the molecular mechanisms underlying the pathogenesis of delayed cognitive dysfunction are not well-defined and effective treatments or prevention measures remain insufficient. In the present study, 60 adult male Wistar rats were randomly divided into three groups, which included a control, whole brain radiotherapy (WBRT) (single dose of 30 Gy of WBRT) and nimodipine (single dose of 30 Gy of WBRT followed by nimodipine injection intraperitoneally) groups. The rats were sacrificed 7 days or 3 months following irradiation. At 3 months, the Morris water maze test was used to assess spatial learning and memory function in rats. The results demonstrated that the WBRT group demonstrated a significantly impaired cognitive performance, decreased numbers of hippocampal Cornu Ammonis (CA)1 neurons and upregulated expression of caspase-3 in the dentate gyrus compared with those in the control and nimodipine groups. Reverse transcription-quantitative polymerase chain reaction analysis demonstrated that the WBRT group exhibited increased ratio of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax)/Bcl-2 compared with that in control and nimodipine groups on day 7 following irradiation. However, the WBRT group exhibited decreased levels of brain-derived neurotrophic factor (BDNF) compared with that in control and nimodipine groups at 3 months following brain irradiation. The levels of growth-associated protein 43 and amyloid precursor protein between the nimodipine group and WBRT group were not statistically significant. The present study demonstrated that neuron apoptosis may lead to delayed cognitive deficits in the hippocampus, in response to radiotherapy. The cognitive impairment may be alleviated in response to a calcium antagonist nimodipine. The molecular mechanisms involved in nimodipine-mediated protection against cognitive decline may involve the regulation of Bax/Bcl-2 and BDNF in the hippocampus.

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Protective effects of nimodipine on cerebrovascular function in chronic alcoholic encephalopathy

Cited by 9 publications

References 29 publications

<p>Tetramethylpyrazine attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells through regulating apoptosis, autophagy and oxidative damage</p>

<p>Tetramethylpyrazine attenuated bupivacaine-induced neurotoxicity in SH-SY5Y cells through regulating apoptosis, autophagy and oxidative damage</p>

Effects of nimodipine on postoperative delirium in elderly under general anesthesia

Delayed cognitive deficits can be alleviated by calcium antagonist nimodipine by downregulation of apoptosis following whole brain radiotherapy

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