Inhibition of PLCβ1 signaling pathway regulates methamphetamine self-administration and neurotoxicity in rats

Xu, Xingshun; Fan, Runyue; Ruan, Yanqian; Xu, Mengjie; He, Jiajie; Cao, Mengye; Li, Xingxing; Zhou, Wenhua; Liu, Yu

doi:10.1016/j.fct.2021.111970

Cited by 10 publications

(3 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…induced oxidative stress, which is prevented by central injection of AT 1 -R blockers or angiotensin-converting enzyme inhibitors ( Bild et al, 2013 ). In line with the present results, Xu et al showed that methamphetamine induces oxidative stress and the associated neurotoxicity by AT 1 -R, via phospholipase C β1 ( Xu et al, 2021 ). As oxidative stress plays a crucial role in the amphetamines-induced neurotoxicity ( Moratalla et al, 2017 ), the above and the present results suggest that AT 1 -R may be involved in neurotoxicity effects of others amphetamines derivatives such as 3,4-methylenedioxymethamphetamine.…”

Section: Discussionsupporting

confidence: 92%

Amphetamine Induces Oxidative Stress, Glial Activation and Transient Angiogenesis in Prefrontal Cortex via AT1-R

et al. 2021

View full text Add to dashboard Cite

Background: Amphetamine (AMPH) alters neurons, glia and microvessels, which affects neurovascular unit coupling, leading to disruption in brain functions such as attention and working memory. Oxidative stress plays a crucial role in these alterations. The angiotensin type I receptors (AT1-R) mediate deleterious effects, such as oxidative/inflammatory responses, endothelial dysfunction, neuronal oxidative damage, alterations that overlap with those observed from AMPH exposure.Aims: The aim of this study was to evaluate the AT1-R role in AMPH-induced oxidative stress and glial and vascular alterations in the prefrontal cortex (PFC). Furthermore, we aimed to evaluate the involvement of AT1-R in the AMPH-induced short-term memory and working memory deficit.Methods: Male Wistar rats were repeatedly administered with the AT1-R blocker candesartan (CAND) and AMPH. Acute oxidative stress in the PFC was evaluated immediately after the last AMPH administration by determining lipid and protein peroxidation. After 21 off-drug days, long-lasting alterations in the glia, microvessel architecture and to cognitive tasks were evaluated by GFAP, CD11b and von Willebrand immunostaining and by short-term and working memory assessment.Results: AMPH induced acute oxidative stress, long-lasting glial reactivity in the PFC and a working memory deficit that were prevented by AT1-R blockade pretreatment. Moreover, AMPH induces transient angiogenesis in PFC via AT1-R. AMPH did not affect short-term memory.Conclusion: Our results support the protective role of AT1-R blockade in AMPH-induced oxidative stress, transient angiogenesis and long-lasting glial activation, preserving working memory performance.

show abstract

Section: Discussionsupporting

confidence: 92%

Amphetamine Induces Oxidative Stress, Glial Activation and Transient Angiogenesis in Prefrontal Cortex via AT1-R

et al. 2021

View full text Add to dashboard Cite

show abstract

“…An increasing body of evidence suggests that METH can cause toxicity by inducing ROS production and redox imbalance ( 23 , 24 ). Besides, ROS induction has been well documented in multiple cancers and may lead to the activation of pro-tumorigenic signaling and induction of genetic instability or DNA damage ( 25 , 26 ).…”

Section: Discussionmentioning

confidence: 99%

An unconventional cancer-promoting function of methamphetamine in hepatocellular carcinoma

Yang

Wang

et al. 2023

Life Sci. Alliance

View full text Add to dashboard Cite

For the past decade, the prevalence and mortality of methamphetamine (METH) use have doubled, suggesting that METH use could be the next substance use crisis worldwide. Ingested METH is transformed into other products in the liver, a major metabolic organ. Studies have revealed that METH causes deleterious inflammatory response, oxidative stress, and extensive DNA damage. These pathological damages are driving factors of hepatocellular carcinoma (HCC). Nonetheless, the potential role of METH in HCC and the underlying mechanisms remain unknown. Herein, we found a higher HCC incidence in METH abusers. METH promoted cellular proliferation, migration, and invasion in two human-derived HCC cells. Consistently, METH uptake promoted HCC progression in a xenograft mouse model. Mechanistically, METH exposure induced ROS production, which activated the Ras/MEK/ERK signaling pathway. Clearance of ROS by NAC suppressed METH-induced activation of Ras/ERK1/2 pathways, leading to arrest of HCC xenograft formation in nude mice. To the best of our knowledge, this is the first study to substantiate that METH promotes HCC progression and inhibition of ROS may reverse this process.

show abstract

“…The same procedure is repeated to obtain the offspring of the second generation (Ganiger et al, 2007; Q. Liu et al, 2018; Montagnini et al, 2018; Wang et al, 2019). Neurotoxicity studies evaluate neuropathological lesions and neurological dysfunctions (loss of memory, sensory defects, and learning and memory dysfunctions) after 28 or 90 days of administration (Ishtiaq et al, 2021; Xu et al, 2021). Embryotoxicity studies evaluate embryofetal effects (hemorrhagic bullae, malformations, deformities, and mortality) between the 8th and 14th day of pregnancy (Carvalho et al, 2020; Maziero et al, 2020).…”

Section: In Vivo Preclinical Studiesmentioning

confidence: 99%

Baseline and time‐updated factors in preclinical development of anionic dendrimers as successful anti‐HIV‐1 vaginal microbicides

Rodriguez-Izquierdo

Sepúlveda‐Crespo

Lasso³

et al. 2022

WIREs Nanomed Nanobiotechnol

View full text Add to dashboard Cite

Although a wide variety of topical microbicides provide promising in vitro and in vivo efficacy, most of them failed to prevent sexual transmission of human immunodeficiency virus type 1 (HIV-1) in human clinical trials. In vitro, ex vivo, and in vivo models must be optimized, considering the knowledge acquired from unsuccessful and successful clinical trials to improve the current gaps and the preclinical development protocols. To date, dendrimers are the only nanotool that has advanced to human clinical trials as topical microbicides to prevent HIV-1 transmission. This fact demonstrates the importance and the potential of these molecules as microbicides. Polyanionic dendrimers

show abstract

Inhibition of PLCβ1 signaling pathway regulates methamphetamine self-administration and neurotoxicity in rats

Cited by 10 publications

References 56 publications

Amphetamine Induces Oxidative Stress, Glial Activation and Transient Angiogenesis in Prefrontal Cortex via AT1-R

Amphetamine Induces Oxidative Stress, Glial Activation and Transient Angiogenesis in Prefrontal Cortex via AT1-R

An unconventional cancer-promoting function of methamphetamine in hepatocellular carcinoma

Baseline and time‐updated factors in preclinical development of anionic dendrimers as successful anti‐HIV‐1 vaginal microbicides

Contact Info

Product

Resources

About