Propofol but not dexmedetomidine produce locomotor sensitization via nitric oxide in rats

Uskur, Tuğçe; Şenöz, Ayşe Özçetin; Çevreli, Burcu; Barlas, A.; Uzbay, Tayfun

doi:10.1007/s00213-020-05707-5

Cited by 6 publications

(7 citation statements)

References 45 publications

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“…Propofol (2,6-diisopropylphenol) is a common hypnotic agent used in many day surgeries and non-operating room anesthetic procedures since it has fewer adverse effects than other anesthetics (Uskur et al 2021). Propofol, on the other hand, is regarded to be safe and possesses antiemetic, anti-pruritic, anxiolytic, bronchodilator, muscle relaxant, and anti-epileptic effects.…”

Section: Introductionmentioning

confidence: 99%

The effects of thiamine pyrophosphate on propofol-induced oxidative liver injury and effect on dysfunction

Delen¹,

Dişli²,

Taş³

et al. 2022

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Propofol may cause an increase in reactive oxygen species in the body. In this study, we tested the effect of antioxidant thiamine pyrophosphate (TPP) on propofol-induced liver damage. The eighteen rats were split into three groups: HG, healthy; PP, propofol-treated (50 mg/kg) and PT, treated with propofol (50 mg/kg) and TPP (25 mg/kg). Total glutathione (tGSH), total oxidant (TOS), and total antioxidant (TAS) levels were tested together with aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and malondialdehyde (MDA). Histopathological examination of the tissues was performed. We have found that levels of MDA, TOS, ALT, AST, and LDH were all higher in PP group than in HG and PT groups (p < 0.05). In PP group, the TAS and tGSH levels were statistically substantially lower. The PT for oxidants levels showed a statistically significant reduction. In PT group, the levels of antioxidants were found to be considerably higher. The epitheliums, glands, and vascular structures of the PTs were histologically close to normal. By boosting antioxidants, TPP may help to reduce propofolinduced liver damage.

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Section: Introductionmentioning

confidence: 99%

The effects of thiamine pyrophosphate on propofol-induced oxidative liver injury and effect on dysfunction

Delen¹,

Dişli²,

Taş³

et al. 2022

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“…First, HIF-1α could stabilize p53, 21 and more severe or long-term hypoxia can cause cell apoptosis through the interaction of HIF and p53. 20 Second, HIF-1α could induce the transcription of several pro-apoptosis genes, including HGTD-P and BNIP3, 22 inhibition of which could exert a protective effect on hepatic IRI. Third, HIF-1α-dependent up-regulation of the transferrin gene promotes ROS production and participates in liver injury during reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Hepatic Ischemia-reperfusion Injury in Mice was Alleviated by Rac1 Inhibition – More Than Just ROS-inhibition

Sha¹,

Yang²,

Liu³

et al. 2021

J Clin Transl Hepatol

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Background and Aims: Reducing reactive oxygen species (ROS) production has proven an effective way for alleviating oxidative stress during ischemia-reperfusion injury (IRI). Moreover, inhibition of Rac1 could reduce ROS production and prevent oxidative stress injury. Previous studies have suggested a positive interactivation feedback loop between Rac1 and hypoxia-inducible factor (HIF)-1α, the latter being up-regulated early during ischemia. The positive inter-activation between Rac1 and HIF-1α would aggravate ROS production, thereby promoting IRI. This study was designed to verify the effects of Rac1 inhibition on hepatic IRI both at animal and cellular levels and to explore the interaction between Rac1 and HIF-1α during hepatic IRI. Methods: C57B/6 mice and AML-12 cells were used for the construction of hepatic IRI animal and cell models. Rac1 inhibition was achieved by NSC23766 (a specific Rac1 inhibitor). Lentiviral vectors were used for Rac1 knockdown. At designated time points, serum and liver tissues were collected from the mice and treated cells were collected for further analysis. Results: NSC23766 treatment significantly alleviated the hepatic IRI in mice, manifesting as lower vacuolation score and less apoptosis cells, lower ROS and serum/liver alanine aminotransferase/aspartate aminotransferase levels, and fewer activated inflammatory cells. IRI of AML-12 was also alleviated by 50 µM NSC23766 or Rac1-knockdown, manifesting as reduced cell apoptosis, less extensive interruption of mitochondrial membrane potential, down-regulation of apoptosis, and effects on DNA damage-related proteins. Interestingly, Rac1 knockdown also down-regulated the expression level of HIF-1α. Conclusions: Our study supports a protective effect of Rac1 inhibition on hepatic IRI. Aside from the classic topics of reducing ROS production and oxidative stress, our study showed an interaction between Rac1 and HIF-1α signaling during hepatic IRI.

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“…Propofol addiction has gradually developed into a major social and health problem since it was firstly reported in 1992 2,3 . Because of its great harm, it is increasingly important for us to explore the underlying mechanisms of propofol addiction in order to prevent and cure propofol abuse 4,5 …”

Section: Introductionmentioning

confidence: 99%

“…2,3 Because of its great harm, it is increasingly important for us to explore the underlying mechanisms of propofol addiction in order to prevent and cure propofol abuse. 4,5 The nucleus accumbens (NAc), a part of ventral striatum in the basal ganglia, which has been shown to be unique for cognitive integration and motivated behaviour, 6 and the subcompartment of NAc shell (NAsh) is indicated to be primarily responsible for driving behavioural responses to repeated reward exposure, including chronic drug administration. 7 Medium spiny neurons (MSNs), a GABAergic neuron that comprises almost 90% of the NAc cell population, receiving convergent synapses and are regulated by dopamine efferent originating ventral tegmental area (VTA) and glutamate inputs from prefrontal cortex and limbic regions.…”

mentioning

confidence: 99%

The excitatory transmission from basolateral nuclues of amygdala to nucleus accumbens shell regulates propofol self‐administration through AMPA receptors

et al. 2023

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Propofol addictive properties have been demonstrated in humans and rats. The glutamatergic transmission from basolateral nucleus of amygdala (BLA) to the nucleus accumbens (NAc) modulates reward-seeking behaviour; especially, NAc shell (NAsh) is implicated in reward-seeking response. Previous studies indicated the interactions between AMPA receptors (AMPARs) and dopamine D1 receptor (D1R) in NAc mediated drug addiction, but whether the circuit of BLA-to-NAsh and AMPARs regulate propofol addiction remains unclear. We trained adult male Sprague-Dawley rats for propofol self-administration to examine the changes of action potentials (APs) and spontaneous excitatory postsynaptic currents (sEPSCs) in the NAsh. Thereafter, optogenetic stimulation with adeno-associated viral vectors microinjections in BLA was used to explore the effect of BLA-to-NAsh on propofol self-administration behaviour (1.7 mg/kg/injection). The pretreatment effects with NBQX (0.25-1.0 μg/0.3 μl/site) or vehicle in the NAsh on propofol self-administration behaviour, the expressions of AMPARs subunits and D1R/ERK/CREB signalling pathway in the NAc were detected. The results showed that the number of APs, amplitude and frequency of sEPSCs were enhanced in propofol self-administrated rats. Propofol selfadministration was inhibited in the NpHR3.0-EYFP group, but in the ChR2-EYFP group, there was a promoting effect, which could be weakened by NBQX pretreatment. NBQX pretreatment also significantly decreased the expressions of GluA2 subunit and D1R in the NAc but did not change the expressions of GluA1 and ERK/CREB signalling pathway. The evidence supports a vital role of BLA-to-NAsh circuit in regulating propofol self-administration and suggests this central reward processing may function through the interaction between AMPARs and D1R in the NAsh.

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Propofol but not dexmedetomidine produce locomotor sensitization via nitric oxide in rats

Cited by 6 publications

References 45 publications

The effects of thiamine pyrophosphate on propofol-induced oxidative liver injury and effect on dysfunction

The effects of thiamine pyrophosphate on propofol-induced oxidative liver injury and effect on dysfunction

Hepatic Ischemia-reperfusion Injury in Mice was Alleviated by Rac1 Inhibition – More Than Just ROS-inhibition

The excitatory transmission from basolateral nuclues of amygdala to nucleus accumbens shell regulates propofol self‐administration through AMPA receptors

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