Ropivacaine impairs mitochondrial biogenesis by reducing PGC-1α

Niu, Zejun; Tang, Jiaming; Ren, Yueyi; Feng, Wei

doi:10.1016/j.bbrc.2018.08.186

Cited by 14 publications

(10 citation statements)

References 22 publications

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“…At the dose used by the authors, 50 mg/ kg by oral gavage every day, the flavone apigenin can induce the early expression of procaspase-3, which is crucial for the activation of mitochondrial biogenesis initiators, such as TFAM and NRF-1 (Kim, Ha, Yang, & Son, 2018). In this perspective, a significant role is ruled by the PGC-1α, the expression of which is particularly stringent for mitochondrial biogenesis (Chen, Tao, Li, & Yao, 2018;Niu, Tang, Ren, & Feng, 2018).…”

Section: Introductionmentioning

confidence: 99%

Is Mitochondria Biogenesis and Neuronal Loss Prevention in Rat Hippocampus Promoted by Apigenin?

Chirumbolo

2019

Basic Clin. Neurosci. J.

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Section: Introductionmentioning

confidence: 99%

Is Mitochondria Biogenesis and Neuronal Loss Prevention in Rat Hippocampus Promoted by Apigenin?

Chirumbolo

2019

Basic Clin. Neurosci. J.

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“…Although there is a report that ropivacaine has the least neurotoxicity among the other LAs including lidocaine and bupivacaine [19,20], the permanent nerve damage from ropivacaine is concerned by many doctors and there lacks some effective preventive and therapeutic measures. However, the molecular mechanism of ropivacaine-induced neurotoxicity remains unclear, but the effect is likely muti-factorial, there are several possibilities have been proposed, including intercellular calcium overload [21][22][23], neuronal mitochondrial dysfunction [24,25], neuronal apoptosis [26,27] and autophagy [10]. Some studies have reported that Ttype calcium channels and its regulatory proteins were intimately involved in ropivacaine-induced neurotoxicity, and the inhibition of those could improve the neurotoxicity from ropivacaine [28].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Attenuates Ropivacaine-Induced Apoptosis by Inhibiting Excessive Mitophagy Through the Parkin/PINK1 Pathway in PC12 and HT22 Cells

Zeng

Liu

et al. 2022

Inflammation

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Melatonin, as an endogenous circadian indoleamine, is secreted from the pineal gland and has extensive biological functions, including antioxidant, anti-in ammatory, anti-tumor and neuroprotective effects. Its neuroprotective effects make it to be a potential therapeutic for many nerve damages, but its effect on ropivacaine-induced neurotoxicity remains unclear. The aims of our research were to explore the impact and mechanism of melatonin on ropivacaine-induced neurotoxicity. Our results shown that melatonin pretreatment protected the cell viability, morphology, and apoptosis of PC12 and HT22 cells from ropivacaine, it also improved ropivacaine-induced mitochondrial dysfunction and it inhibited an increase of mitophagy levels by ropivacaine. In addition, our study also revealed that the increase of mitophagy levels could reduce the protective effect of melatonin on ropivacaine-induced apoptosis in PC12 and HT22 cells, but the inhibition of mitophagy could enhance this effect of melatonin. To further illustrate the mechanism of melatonin inhibited mitophagy, the expressions of Parkin and PINK1 were detected, and results shown that melatonin inhibited the activation of Parkin / PINK1 pathway. In conclusion, our results indicated that melatonin protected ropivacaine-induced apoptosis through suppressing excessive mitophagy by inhibiting the Parkin / PINK1 pathway. Melatonin may be a useful potential therapeutic agent against ropivacaine-induced neurotoxicity.

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“…In addition to the Fas/FasL pathway, some investigators have reported that RH can reduce the mitochondrial membrane potential of human neuroblastoma SH-5Y5Y cells, which decreases the cytochrome C activity and ATP production, thereby activating caspase-3 to induce apoptosis (21). Niu et al revealed that RH reduced the expression of major mitochondrial regulator peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1a) and its downstream transcription factors, then inducing the loss of mitochondrial function (22).…”

Section: Rh Increased Protein Expression Of Fas Fasl and Cleaved Camentioning

confidence: 99%

Repeated Intrathecal Administration of Ropivacaine Hydrochloride Induces Apoptosis Via Up-Regulating of Fas/FasL Expression in the Rat Spinal Cord

Zhang

Zeng

Luo

et al. 2020

Preprint

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Background: Ropivacaine hydrochloride (RH) is a local anesthetic and frequently used for perioperative anesthesia and analgesia; but it has potential neurotoxicity, especially when intrathecally used repeatedly for a long time, although the exact mechanism is unclear.Methods: In this study, the expression of Factor associated suicide receptor (Fas) and its ligand (FasL) in the spinal cord cells was detected in rats receiving repeated intrathecal injection of RH. The paw mechanical withdraw threshold (MWT) was measured before and 3 days after intrathecal cannulation and 24 h after intrathecal administration. Rats received intrathecal injection of 0.5%, 1%, 2% RH at 0.12 ml/kg or saline of equal volume alone. Intrathecal injection was done 8 times with an interval of 1.5h in 12 h. The spinal cord was collected for pathological examination; TUNEL staining was used to assess the apoptosis in the spinal cord and the expression of Fas, FasL, caspase-3, and caspase-8 was detected by qPCR and Western blotting.Results: 1% and 2% RH groups significantly increased the MWT (P<0.05) and more vacuoles or edema was observed in the spinal cord after RH treatment. The apoptosis rates and expression of Fas, FasL, caspase-3, and caspase-8 increased in the RH groups (P<0.05).Conclusions: Repeated intrathecal administration of RH may cause damage to the spinal cord and induce apoptosis in the spinal cord via up-regulating Fas/FasL expression.

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Ropivacaine impairs mitochondrial biogenesis by reducing PGC-1α

Cited by 14 publications

References 22 publications

Is Mitochondria Biogenesis and Neuronal Loss Prevention in Rat Hippocampus Promoted by Apigenin?

Is Mitochondria Biogenesis and Neuronal Loss Prevention in Rat Hippocampus Promoted by Apigenin?

Melatonin Attenuates Ropivacaine-Induced Apoptosis by Inhibiting Excessive Mitophagy Through the Parkin/PINK1 Pathway in PC12 and HT22 Cells

Repeated Intrathecal Administration of Ropivacaine Hydrochloride Induces Apoptosis Via Up-Regulating of Fas/FasL Expression in the Rat Spinal Cord

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