Protective role of lidocaine against cerebral ischemia‑reperfusion injury: An <i>in vitro</i> study

Lan, Xiaoyang; Xu, Youyong

doi:10.3892/etm.2021.10964

Cited by 4 publications

(5 citation statements)

References 39 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results of the present study determined that lidocaine protected against LIRI in H/R-induced A549 cells. Evidently, lidocaine can exert protective effects on IR injury in various diseases, such as ischemic brain damage, ischemic spinal cord and myocardial injury ( 31 – 33 ). Of note, it has been found that lidocaine can inhibit the process of apoptosis under multiple pathological states, such as cerebral I/R injury and myocardial damage due to ischemia and reperfusion ( 34 , 35 ), consistent with the findings in the present study.…”

Section: Discussionmentioning

confidence: 99%

Lidocaine attenuates hypoxia/reoxygenation‑induced inflammation, apoptosis and ferroptosis in lung epithelial cells by regulating the p38 MAPK pathway

Yan

2022

Mol Med Rep

View full text Add to dashboard Cite

Lung ischemia-reperfusion (I/R) injury poses a serious threat to human health, worldwide. The current study aimed to determine the role of lidocaine in A549 cells, in addition to the involvement of the p38 MAPK pathway. Oxygen deprivation/reoxygenation-induced A549 cells were utilized to simulate I/R injury in vitro . Cell viability and apoptosis were detected using MTT and TUNEL assays, respectively. The levels of IL-6, IL-8, TNF-α, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase, iron and reactive oxygen species (ROS) were measured using corresponding commercial kits. The corresponding protein expression levels were also measured using western blotting. Moreover, a monolayer cell paracellular permeability assay was performed to determine the permeability of A549 cells. The results demonstrated that, whilst lidocaine had no influence on untreated A549 cells, it significantly increased the viability of hypoxia/reoxygenation (H/R)-induced A549 cells. A549 cell apoptosis and the release of inflammatory cytokines in the H/R group were decreased after the addition of lidocaine. When compared with the H/R group, increased MDA level and decreased SOD level were observed in H/R-induced A549 cells following lidocaine treatment. In addition, the permeability of H/R-induced A549 cells was markedly decreased following lidocaine treatment. Compared with the H/R group, the expression levels of tight junction and ferroptosis-related proteins were significantly upregulated by lidocaine, whereas the expression of transferrin was downregulated. However, p79350, an agonist of p38, reversed the effects of lidocaine on H/R-induced A549 cells. In conclusion, lidocaine exerted a protective role in HR-induced lung epithelial cell injury, which may serve as a potential agent for the treatment of patients with lung I/R injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Lidocaine attenuates hypoxia/reoxygenation‑induced inflammation, apoptosis and ferroptosis in lung epithelial cells by regulating the p38 MAPK pathway

Yan

2022

Mol Med Rep

View full text Add to dashboard Cite

show abstract

“…In addition, IV lidocaine before induction was used to diminish the coughing reflex, as described in humans and dogs 11,12 . Systemic lidocaine also has neuroprotective properties, 13 which could add further interest in the present case. In the present case, lidocaine was administered IV 3 minutes before ketamine and improved the quality of sedation before ketamine administration, which resulted in a smooth induction and orotracheal intubation.…”

Section: Discussionmentioning

confidence: 95%

Management of neuroanaesthesia in a ewe undergoing craniotomy for coenurosis cyst removal

Gavet,

Frikha,

Junot

2023

Vet Record Case Reports

View full text Add to dashboard Cite

Coenurosis is a parasitic disease affecting the central nervous system of small ruminants. This case describes the anaesthetic management of a ewe undergoing craniotomy for associated‐brain cyst removal. As small ruminants are food‐producing animals, there is limited access to veterinary medicinal products, and choosing an appropriate anaesthetic protocol is challenging. After premedication with detomidine (0.03 mg/kg intramuscularly) and butorphanol (0.1 mg/kg intravenously), anaesthesia was induced with lidocaine (1 mg/kg) and ketamine (2 mg/kg intravenously), and maintained with isoflurane in oxygen, using controlled mechanical ventilation. The animal was placed in sternal recumbency, with the head slightly elevated. A lidocaine incisional infiltration was performed, and dexamethasone (0.06 mg/kg intravenously) was administered. Vital parameters remained stable throughout anaesthesia, but moderate agitation was noticed at recovery, treated with butorphanol (0.05 mg/kg intravenously). While the ewe showed clinical improvement initially, its neurological status deteriorated in the following days, leading to euthanasia. Postmortem examination revealed intracranial haematoma.

show abstract

“…Apoptosis, a programmed cell death process, is involved in the pathogenesis of intestinal ischemia-reperfusion injury (30)(31)(32). The ratio of Bax/Bcl-2 is known to reflect the status of apoptosis, and its role in IRI has recently received widespread attention (8,33). Accumulating evidence indicates that intestinal I/R significantly increases the Bax/Bcl-2 ratio, which leads to impaired cell survival and tissue repair (8,34,35).…”

Section: Discussionmentioning

confidence: 99%

“…The ratio of Bax/Bcl-2 is known to reflect the status of apoptosis, and its role in IRI has recently received widespread attention (8,33). Accumulating evidence indicates that intestinal I/R significantly increases the Bax/Bcl-2 ratio, which leads to impaired cell survival and tissue repair (8,34,35). On the other hand, several studies have also implicated that reducing the activity of the Bax/Bcl-2 axis may be advantageous for intestinal protection and repair IRI (36–38).…”

Section: Discussionmentioning

confidence: 99%

“…Intestinal ischemia-reperfusion injury is a complex pathological process that involves various cellular responses, including apoptosis. Bax/Bcl-2 proteins are known to be key regulators of apoptosis, and their abnormal expression and activity play a crucial role in the pathogenesis of IRI (8)(9)(10). Parkin is an E3 ubiquitin ligase with diverse roles in mitochondrial homeostasis and cell signaling pathways (11,12).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Prmt6-Foxo3a Attenuates Apoptosis by Upregulating Parkin Expression in Intestinal Ischemia-Reperfusion Injury

Wu,

Zhou,

et al. 2024

Shock

View full text Add to dashboard Cite

Intestinal ischemia-reperfusion injury (IIRI) is a serious disease with high morbidity and mortality. This study aims to investigate the potential regulatory mechanisms involving protein arginine methyltransferase 6 (PRMT6), Forkhead box O3a (FoxO3a), and Parkin in IIRI and elucidate their roles in mediating cell apoptosis. The IIRI animal model was established and confirmed using Hematoxylin and Eosin (H&E) staining. Oxygen-glucose deprivation and reperfusion (OGD/R) cell model was established to mimic ischemic injury in vitro. Transient transfection was used to overexpress or knock down genes. Cell death or apoptosis was assessed by propidium iodide staining, TUNEL assay, and flow cytometry. The expression of proteins was detected by Western blot. The histopathology observed by HE staining suggested that the IIRI animal model was successfully established. Our findings revealed that IIRI resulted in increased Bax and decreased Bcl-2 levels. In vitro experiments showed that overexpression of Parkin decreased OGD/R injury and suppressed elevation of Bax/Bcl-2. PRMT6 regulated the methylation level of FoxO3a. Moreover, FoxO3a directly binds to Parkin, and FoxO3a overexpression reduced OGD/R-induced cell death and regulation of Parkin. Overexpression of PRMT6 can attenuate the downregulation of Parkin and elevation of Bax/Bcl-2 caused by OGD/R. Knockdown of PRMT6 promoted apoptosis in intestinal epithelial cells of OGD/R group, while PRMT6 overexpression exhibited the opposite effect. Notably, the levels of PRMT6, FoxO3a, and Parkin were decreased in IIRI mouse intestinal tissue. Knocking out PRMT6 causes a significant decrease in the lifespan of mice. Altogether, our results demonstrated that PRMT6 upregulated the expression of Parkin by regulating FoxO3a methylation level, attenuating the apoptosis induced by IIRI.

show abstract

Protective role of lidocaine against cerebral ischemia‑reperfusion injury: An in vitro study

Cited by 4 publications

References 39 publications

Lidocaine attenuates hypoxia/reoxygenation‑induced inflammation, apoptosis and ferroptosis in lung epithelial cells by regulating the p38 MAPK pathway

Lidocaine attenuates hypoxia/reoxygenation‑induced inflammation, apoptosis and ferroptosis in lung epithelial cells by regulating the p38 MAPK pathway

Management of neuroanaesthesia in a ewe undergoing craniotomy for coenurosis cyst removal

Prmt6-Foxo3a Attenuates Apoptosis by Upregulating Parkin Expression in Intestinal Ischemia-Reperfusion Injury

Contact Info

Product

Resources

About