Evaluation of sciatic nerve damage following intraneural injection of bupivacaine, levobupivacaine and lidocaine in rats

Şen, Öznur; Sayilgan, Nevzat; Tütüncü, Ayşe Çiğdem; Bakan, Mefkür; Köksal, Güniz Meyancı; Öz, Hüseyin

doi:10.1016/j.bjane.2014.09.012

Cited by 12 publications

(9 citation statements)

References 6 publications

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“…Immediately after the isolation of brain samples were fixed in 10% phosphate‐buffered formaldehyde, embedded in paraffin and 5‐μm longitudinal sections were performed after crossing of hippocampus and prefrontal cortex region. Sections of hippocampus and prefrontal cortex were stained with haematoxylin and eosin (H&E) and examined microscopically …”

Section: Methodsmentioning

confidence: 99%

Molecular mechanism of tuberoinfundibular peptide of 39 on glucocorticoid receptor mediated glutamate/GABA imbalance and cerebral abnormalities against cognitive deficit model

Gunasekaran¹,

Sankar

Ramanathan³

2019

Journal of Pharmacy and Pharmacology

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Objectives This study is designed to evaluate the role of tuberoinfundibular peptide of 39 (TIP39) in connection with glucocorticoid receptor‐mediated glutamate/GABA abnormalities in chronic unpredictable mild stress (CUMS) model. Methods Male Sprague–Dawley rats were treated with TIP39 (1 and 10 nmol, i.c.v) and diazepam 2 mg/kg throughout the stress period (28 days) in alternate days. Then, rats were subjected for different behavioural activity followed by biochemical, gene expression and histological examinations. Key findings Chronic unpredictable mild stress rats showed significant cognitive impairment in Morris water maze, Novel object recognition and Y maze test. This was reversed after TIP39 administration. Moreover, TIP39 significantly decreased the brain glutamate and acetyl cholinesterase levels in CUMS rats, whereas it increases the level of GABA after TIP39 treatment. These changes were evident with increased glutamic acid decarboxylase enzyme activity by TIP39. TIP39 significantly decreased the brain glucocorticoid and mineralocorticoid receptor expression ratio in comparison with CUMS rats. Moreover, histological abnormalities in prefrontal cortex and hippocampus were markedly improved after TIP39 administration in CUMS rats. Conclusions Tuberoinfundibular peptide of 39 can be a potent neuroendocrine modulator in treating cognitive impairment induced by CUMS rats by controlling glucocorticoid receptor‐mediated glutamate/GABA abnormalities in brain.

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Section: Methodsmentioning

confidence: 99%

Molecular mechanism of tuberoinfundibular peptide of 39 on glucocorticoid receptor mediated glutamate/GABA imbalance and cerebral abnormalities against cognitive deficit model

Gunasekaran¹,

Sankar

Ramanathan³

2019

Journal of Pharmacy and Pharmacology

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“…However, local anesthesia can also lead to complications, resulting in inevitable adverse effects. Local anesthesia affects the central nervous system and the cardiovascular system and may therefore lead to neurotoxicity [ 2 ], resulting in nerve injuries and pathological changes in the peripheral nerves. Deaths from local anesthesia are mainly attributed to adverse effects on the cardiovascular system, which include contractile dysfunction and cardiac arrhythmia [ 3 ], and are mainly characterized by hemodynamic changes [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture pretreatment alleviates myocardial injury through regulating mitochondrial function

et al. 2020

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Background: Electroacupuncture is well known for its advantageous neuroanalgesic and therapeutic effects on myocardial ischemia-reperfusion injury. The purpose of the present research was to verify whether electroacupuncture can alleviate bupivacaine-induced myocardial injury. Methods: Specific pathogen-free Wistar rats were used to establish the bupivacaine-induced myocardial injury model. Western blot, PCR, transmission electron microscope and enzyme-linked immunosorbent (ELISA) methods were used to evaluate bupivacaine-induced structure injury and dysfunction of the mitochondria as well as the alleviating effects of lipid emulsion, acupoint injection, and electroacupuncture pre-treatment of the oxidase stress response. Results: Bupivacaine caused structural damage, degradation, and swelling of mitochondria. Furthermore, it reduced adenosine triphosphate (ATP) synthesis and impaired energy metabolism in the mitochondria. Structural and functional impairment of the mitochondria was alleviated via lipid emulsion injection, acupoint injection, and electroacupuncture pre-treatment. Electroacupuncture pre-treatment of PC6 yielded a greater alleviating effect than others approaches. Following electroacupuncture pre-treatment of PC6 point, the number of mitochondria increased; apoptosis was reduced, enzymatic activity of cytochrome C oxidase (COX) and superoxide dismutase and expression of uncoupling protein 2, voltage-dependent anion channel 1, and Bcl 2 were upregulated and SLC25A6, MDA levels were downregulated. Additionally, our findings indicated that electroacupuncture pre-treatment of PC6 point exerted an effect on the mitochondria via the mitochondrial-transcription-factor-A/nuclear-respiratory-factor-1/proliferatoractivated-receptor-gamma-coactivator-1 pathway. Conclusion: The present study revealed that electroacupuncture pre-treatment of PC6 could effectively alleviate bupivacaine-induced myocardial mitochondrial damage, thereby providing a theoretical basis for clinical studies and applications of this treatment method.

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“…A recent study indicated that 5% Bup can induce histopathological abnormalities in a rat model 4. Meanwhile, injection of Bup can also lead to serious sciatic nerve damage in rats 5. Even with a normal or lower dose, Bup can induce neurotoxicity in cells 6.…”

Section: Introductionmentioning

confidence: 99%

<p>Andrographolide attenuates bupivacaine-induced cytotoxicity in SH-SY5Y cells through preserving Akt/mTOR activity</p>

Zhang¹,

Wang²,

Du³

2019

DDDT

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Background: Bupivacaine (Bup) is the most commonly used local anesthetic. However, Bup induces cytotoxicity, especially in older patients. Recent reports have indicated that andrographolide (Andro) exhibits protective effects on human neurons. Nevertheless, whether Andro can inhibit Bup-induced cytotoxicity remains unclear. As such, we investigated the effect of Andro on Bup-induced cytotoxicity of SH-SY5Y cells in the present study. Methods: Western blotting was used to examine expression of Bax, Bcl2, active caspase 3, p-Akt, and p-mTOR in SH-SY5Y cells. In addition, ELISA was used to detect levels of total glutathione and reactive oxygen species in cells. Results: We found that Andro attenuated Bup-induced cytotoxicity of SH-SY5Y cells. In addition, Andro inhibited Bup-induced apoptosis via downregulating the expression of Bax and active caspase 3 and upregulating the proteins Bcl2, p-Akt, and p-mTOR in SH-SY5Y cells. Moreover, Andro alleviated Bup-induced oxidative damage in SH-SY5Y cells via downregulating the level of reactive oxygen species and upregulating of the level of total glutathione. More significantly, inhibition of Akt abolished the protective effect of Andro in Bup-treated SH-SY5Y cells. Conclusion: Our findings indicated that Andro played a neuroprotective role via preserving Akt/mTOR activity and increasing antioxidative status in Bup-treated SH-SY5Y cells. Therefore, Andro may be a potential agent for the treatment of human cytotoxicity induced by Bup.

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Evaluation of sciatic nerve damage following intraneural injection of bupivacaine, levobupivacaine and lidocaine in rats

Abstract: In all groups, histopathological damage frequency and severity were more than the motor deficiency.

Cited by 12 publications

References 6 publications

Molecular mechanism of tuberoinfundibular peptide of 39 on glucocorticoid receptor mediated glutamate/GABA imbalance and cerebral abnormalities against cognitive deficit model

Molecular mechanism of tuberoinfundibular peptide of 39 on glucocorticoid receptor mediated glutamate/GABA imbalance and cerebral abnormalities against cognitive deficit model

Electroacupuncture pretreatment alleviates myocardial injury through regulating mitochondrial function

<p>Andrographolide attenuates bupivacaine-induced cytotoxicity in SH-SY5Y cells through preserving Akt/mTOR activity</p>

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