Ropivacaine- and bupivacaine-induced death of rabbit annulus fibrosus cells in vitro : involvement of the mitochondrial apoptotic pathway

Cai, Xianyi; Xia, Yun; Yang, Shuo; Liu, X.-Z.; Shao, Zengwu; Liu, Y.-L.; Yang, Wei; Xiong, Liming

doi:10.1016/j.joca.2015.05.013

Cited by 45 publications

(56 citation statements)

References 40 publications

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“…Previous finding suggested that LAs in clinically relevant doses could evoke apoptosis of rabbit AF cells, involving, at least in part, the mitochondrial pathway32. Calcium is well known to be an important second messenger in the regulation of many cellular physiological functions, and calcium overload is harmful to mitochondrial function.…”

Section: Discussionmentioning

confidence: 99%

Neurotoxicity Comparison of Two Types of Local Anaesthetics: Amide-Bupivacaine versus Ester-Procaine

Zhao

et al. 2017

Sci Rep

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Local anaesthetics (LAs) may lead to neurological complications, but the underlying mechanism is still unclear. Many neurotoxicity research studies have examined different LAs, but none have comprehensively explored the distinct mechanisms of neurotoxicity caused by amide- (bupivacaine) and ester- (procaine) type LAs. Here, based on a CCK8 assay, LDH assay, Rhod-2-AM and JC-1 staining, 2′,7′-dichlorohy-drofluorescein diacetate and dihydroethidium probes, an alkaline comet assay, and apoptosis assay, we show that both bupivacaine and procaine significantly induce mitochondrial calcium overload and a decline in the mitochondrial membrane potential as well as overproduction of ROS, DNA damage and apoptosis (P < 0.05). There were no significant differences in mitochondrial injury and apoptosis between the bupivacaine and procaine subgroups (P > 0.05). However, to our surprise, the superoxide anionic level after treatment with bupivacaine, which leads to more severe DNA damage, was higher than the level after treatment with procaine, while procaine produced more peroxidation than bupivacaine. Some of these results were also affirmed in dorsal root ganglia neurons of C57 mice. The differences in the superoxidation and peroxidation induced by these agents suggest that different types of LAs may cause neurotoxicity via different pathways. We can target more accurate treatment based on their different mechanisms of neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

Neurotoxicity Comparison of Two Types of Local Anaesthetics: Amide-Bupivacaine versus Ester-Procaine

Zhao

et al. 2017

Sci Rep

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“…The cell counting kit-8 was applied to determine viability of osteoblastic cells and bone marrow-derived MSCs as described previously (Ding et al, 2012; Cai et al, 2015). After exposure to FAC (25–200 µM) for 24 and 120 h, the mixture solution containing medium (90 µl) and CCK-8 reactant (10 µl) was added to each well of a 96-well plate.…”

Section: Methodsmentioning

confidence: 99%

“…After treatment as described above, osteoblasts and bone marrow-derived MSCs from each sample were stained using the Annexin V–FITC/PI kit, as described previously (Ding et al, 2012; Cai et al, 2015). Then, flow cytometry was accomplished by flow cytometric analysis (BD, USA).…”

Section: Methodsmentioning

confidence: 99%

“…To verify apoptosis, Ding (Ding et al, 2012; Cai et al, 2015) outlined a procedure for ascertaining apoptosis, through the application of Hoechst 33258 dye at 0.5 µg/mL concentrate, to clarify the fractured and compressed apoptotic nuclei. Following the application of the dye, the nuclei were stained for one hour at 37 °C with all light sources omitted.…”

Section: Methodsmentioning

confidence: 99%

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Iron overload induced death of osteoblasts in vitro: involvement of the mitochondrial apoptotic pathway

Tian

Dai

et al. 2016

PeerJ

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BackgroundIron overload is recognized as a new pathogenfor osteoporosis. Various studies demonstrated that iron overload could induce apoptosis in osteoblasts and osteoporosis in vivo. However, the exact molecular mechanisms involved in the iron overload-mediated induction of apoptosis in osteoblasts has not been explored.PurposeIn this study, we attempted to determine whether the mitochondrial apoptotic pathway is involved in iron-induced osteoblastic cell death and to investigate the beneficial effect of N-acetyl-cysteine (NAC) in iron-induced cytotoxicity.MethodsThe MC3T3-E1 osteoblastic cell line was treated with various concentrations of ferric ion in the absence or presence of NAC, and intracellular iron, cell viability, reactive oxygen species, functionand morphology changes of mitochondria and mitochondrial apoptosis related key indicators were detected by commercial kits. In addition, to further explain potential mechanisms underlying iron overload-related osteoporosis, we also assessed cell viability, apoptosis, and osteogenic differentiation potential in bone marrow-derived mesenchymal stemcells(MSCs) by commercial kits.ResultsFerric ion demonstrated concentration-dependent cytotoxic effects on osteoblasts. After incubation with iron, an elevation of intracelluar labile iron levels and a concomitant over-generation of reactive oxygen species (ROS) were detected by flow cytometry in osteoblasts. Nox4 (NADPH oxidase 4), an important ROS producer, was also evaluated by western blot. Apoptosis, which was evaluated by Annexin V/propidium iodide staining, Hoechst 33258 staining, and the activation of caspase-3, was detected after exposure to iron. Iron contributed to the permeabilizatio of mitochondria, leading to the release of cytochrome C (cyto C), which, in turn, induced mitochondrial apoptosis in osteoblasts via activation of Caspase-3, up-regulation of Bax, and down-regulation of Bcl-2. NAC could reverse iron-mediated mitochondrial dysfunction and blocked the apoptotic events through inhibit the generation of ROS. In addition, iron could significantly promote apoptosis and suppress osteogenic differentiation and mineralization in bone marrow-derived MSCs.ConclusionsThese findings firstly demonstrate that the mitochondrial apoptotic pathway involved in iron-induced osteoblast apoptosis. NAC could relieved the oxidative stress and shielded osteoblasts from apoptosis casused by iron-overload. We also reveal that iron overload in bone marrow-derived MSCs results in increased apoptosis and the impairment of osteogenesis and mineralization.

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“…ROS accumulation has been shown to induce NP cell apoptosis through the mitochondrial apoptosis pathway and the death receptor pathway [12][13][14]. Additionally, many external stimuli can cause intracellular ROS accumulation, such as mechanical overloading, nutrition deprivation, and inflammatory cytokines [15,16]. The findings above indicate that oxidative stress-induced NP cell apoptosis may play an important role in disc degeneration.…”

Section: Introductionmentioning

confidence: 93%

Aquaporin-3 Attenuates Oxidative Stress-Induced Nucleus Pulposus Cell Apoptosis Through Regulating the P38 MAPK Pathway

Yao

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Previous studies have shown that oxidative damage is a main contributor to disc nucleus pulposus (NP) cell apoptosis. Aquaporin-3 (AQP-3) facilitates reactive oxygen species (ROS) scavenging and thus alleviates oxidative injury in other cells. This study aims to investigate the role and mechanism of AQP-3 in regulating NP cell apoptosis under oxidative damage. Methods: Rat NP cells were treated with H₂O₂ for 48 hours, while control NP cells were free of H₂O₂. Recombinant AQP-3 lentiviral vectors were used to investigate the effect of enhanced AQP-3 expression levels in NP cells. NP cell apoptosis was assessed by flow cytometry, caspase-3 activity, gene expression of apoptosis-related molecules (Bax, Bcl-2 and caspase-3), and protein expression of cellular apoptosis markers (cleaved PARP and cleaved caspase-3). Additionally, intracellular ROS content and activity of the p38 MAPK pathway were evaluated. Results: Compared with the control NP cells, oxidative damage in the treatment cells significantly increased cell apoptosis ratios and caspase-3 activity, upregulated gene expression of Bax and caspase-3, downregulated gene expression of Bcl-2, and increased protein expression of cleaved PARP and cleaved caspase-3, as well as increased intracellular ROS content and activity of the p38 MAPK pathway. However, AQP-3 overexpression partly alleviated cell apoptosis, decreased intracellular ROS content, and inhibited the p38 MAPK pathway in NP cells under oxidative damage. Conclusion: Oxidative damage can significantly downregulate AQP-3 expression. Enhancing AQP-3 expression in NP cells partly attenuates cellular apoptosis through regulating the p38 MAPK pathway under oxidative damage.

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Ropivacaine- and bupivacaine-induced death of rabbit annulus fibrosus cells in vitro : involvement of the mitochondrial apoptotic pathway

Cited by 45 publications

References 40 publications

Neurotoxicity Comparison of Two Types of Local Anaesthetics: Amide-Bupivacaine versus Ester-Procaine

Neurotoxicity Comparison of Two Types of Local Anaesthetics: Amide-Bupivacaine versus Ester-Procaine

Iron overload induced death of osteoblasts in vitro: involvement of the mitochondrial apoptotic pathway

Aquaporin-3 Attenuates Oxidative Stress-Induced Nucleus Pulposus Cell Apoptosis Through Regulating the P38 MAPK Pathway

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