Is there any therapeutic value for the use of histone deacetylase inhibitors for chronic pain?

Wang, Wei; Cui, Shan; Ling, Rui; Zhang, Hui

doi:10.1016/j.brainresbull.2016.04.010

Cited by 20 publications

(16 citation statements)

References 100 publications

(162 reference statements)

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“…Suberoylanilide hydoxamic acid (SAHA, 40 mg/kg in 1% DMSO; Cayman Chemical, Ann Arbor, Michigan, USA) [41, 42], trichostatin A (TSA, 1 mg/kg in 1% DMSO; Cayman Chemical, Ann Arbor, MI, USA) [43], dacinostat (LAQ824, 10 mg/kg in 1% DMSO; Cayman Chemical, Ann Arbor, MI, USA) [44], entinostat (MS-275, 40 mg/kg in 1% DMSO; Selleck Chemicals, Houston, TX, USA) [45], sodium butyrate (160 mg/kg in saline; Sigma-Aldrich, St. Louis, MO, USA) [46], 4-phenylbutyric acid (4-PBA, 500 mg/kg in 1% DMSO; Sigma-Aldrich) [47, 48], and VPA (200 mg/kg in saline; Cayman Chemical, Ann Arbor, MI, USA) [49] were administered intraperitoneally 1 hour after CFA injection and once daily for 3 days, and control rats received saline or 1% DMSO as vehicle injection. Animals received HDACIs or vehicle (1% DMSO) via intraperitoneal injection daily for 3 days.…”

Section: Methodsmentioning

confidence: 99%

Comparison of Different Histone Deacetylase Inhibitors in Attenuating Inflammatory Pain in Rats

Mao

Zhou

Liu

et al. 2019

Pain Research and Management

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Histone deacetylase inhibitors (HDACIs), which interfere with the epigenetic process of histone acetylation, have shown analgesic effects in animal models of persistent pain. The HDAC family comprises 18 genes; however, the different effects of distinct classes of HDACIs on pain relief remain unclear. The aim of this study was to determine the efficacy of these HDACIs on attenuating thermal hyperalgesia in persistent inflammatory pain. Persistent inflammatory pain was induced by injecting Complete Freund’s Adjuvant (CFA) into the left hind paw of rats. Then, HDACIs targeting class I (entinostat (MS-275)) and class IIa (sodium butyrate, valproic acid (VPA), and 4-phenylbutyric acid (4-PBA)), or class II (suberoylanilide hydoxamic acid (SAHA), trichostatin A (TSA), and dacinostat (LAQ824)) were administered intraperitoneally once daily for 3 or 4 days. We found that the injection of SAHA once a day for 3 days significantly attenuated CFA-induced thermal hyperalgesia from day 4 and lasted 7 days. In comparison with SAHA, suppression of hyperalgesia by 4-PBA peaked on day 2, whereas that by MS-275 occurred on days 5 and 6. Fatigue was a serious side effect seen with MS-275. These findings will be beneficial for optimizing the selection of specific HDACIs in medical fields such as pain medicine and neuropsychiatry.

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Section: Methodsmentioning

confidence: 99%

Comparison of Different Histone Deacetylase Inhibitors in Attenuating Inflammatory Pain in Rats

Mao

Zhou

Liu

et al. 2019

Pain Research and Management

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“…Research on epigenetic modulation has shown that algesia-related synaptic plasticity is regulated by changes in histone acetylation levels and HDAC activity. Hence, HDACs play an important role in the development and persistence of chronic pain [35]. Denk et al found that the intrathecal delivery of various class I HDACIs and antiretroviral drugs (stavudine, d4T) into the spinal cords of rats with traumatic nerve injury induced peripheral neuropathy.…”

Section: Discussionmentioning

confidence: 99%

MiR-34a affects dexmedetomidine-inhibited chronic inflammatory visceral pain by targeting to HDAC2

Liang¹,

Shao²,

Tang³

et al. 2019

BMC Anesthesiol

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Background Dexmedetomidine (DEX) has been used as an anesthetic for decades. The present investigation aimed to elucidate the analgesic impact of DEX on 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced chronic inflammatory visceral pain (CIVP) in rats. Methods TNBS with or without DEX to Male Sprague-Dawley SD rats were randomly divided into four groups: normal, CIVP, DEX, and vehicle. Pain behaviors were assessed and the abdominal withdrawal reflex, mechanical withdrawal threshold, and thermal withdrawal latency were recorded. Quantitative polymerase chain reaction data showed increased expressions of pro-inflammatory cytokines (IL-6, IL-1β and TNF-α) in the spinal cord tissues of rats. Results RNA microarray and quantitative polymerase chain reaction results indicated that miR-34a was downregulated by TNBS induction, but it was upregulated by DEX administration. Further studies showed that transfection of adenovirus-miR-34a inhibitor reversed the effect of DEX on the pain behaviors and spinal-cord pro-inflammatory-cytokine generation in CIVP rats. Additionally, we found that miR-34a targeted the 3′-UTR of the HDAC2 gene, as evinced by the increased HDAC2 expression in the CIVP and DEX + miR-34a inhibitor groups, and decreased HDAC2 signaling in the DEX group. Moreover, knock-down of HDAC2 restored DEX-attenuated pain behaviors and reduced pro-inflammatory cytokine production. Conclusions DEX thus exhibited an analgesic effect on CIVP rats through the miR-34a-mediated HDAC2 pathway and suppressed visceral hypersensitivity.

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“…HDAC inhibitors belong to a large and diverse family of compounds with beneficial effects in a wide range of animal disease models, including glutamate excitotoxicity (Marinova et al 2009 ), chronic pain (Wang et al 2016 ), and atrial fibrillation (Lkhagva et al 2016 ). Furthermore, chromatin modifiers and especially HDAC inhibitors are currently used as drugs for human diseases, such as cancer (Roche and Bertrand 2016 ), diabetes (Arguelles et al 2016 ), and neurological disorders (Falkenberg and Johnstone 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Chaperone co-inducer BGP-15 inhibits histone deacetylases and enhances the heat shock response through increased chromatin accessibility

Budzyński

Crul

Himanen

et al. 2017

Cell Stress and Chaperones

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Defects in cellular protein homeostasis are associated with many severe and prevalent pathological conditions such as neurodegenerative diseases, muscle dystrophies, and metabolic disorders. One way to counteract these defects is to improve the protein homeostasis capacity through induction of the heat shock response. Despite numerous attempts to develop strategies for chemical activation of the heat shock response by heat shock transcription factor 1 (HSF1), the underlying mechanisms of drug candidates’ mode of action are poorly understood. To lower the threshold for the heat shock response activation, we used the chaperone co-inducer BGP-15 that was previously shown to have beneficial effects on several proteinopathic disease models. We found that BGP-15 treatment combined with heat stress caused a substantial increase in HSF1-dependent heat shock protein 70 (HSPA1A/B) expression already at a febrile range of temperatures. Moreover, BGP-15 alone inhibited the activity of histone deacetylases (HDACs), thereby increasing chromatin accessibility at multiple genomic loci including the stress-inducible HSPA1A. Intriguingly, treatment with well-known potent HDAC inhibitors trichostatin A and valproic acid enhanced the heat shock response and improved cytoprotection. These results present a new pharmacological strategy for restoring protein homeostasis by inhibiting HDACs, increasing chromatin accessibility, and lowering the threshold for heat shock response activation.Electronic supplementary materialThe online version of this article (doi:10.1007/s12192-017-0798-5) contains supplementary material, which is available to authorized users.

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Is there any therapeutic value for the use of histone deacetylase inhibitors for chronic pain?

Cited by 20 publications

References 100 publications

Comparison of Different Histone Deacetylase Inhibitors in Attenuating Inflammatory Pain in Rats

Comparison of Different Histone Deacetylase Inhibitors in Attenuating Inflammatory Pain in Rats

MiR-34a affects dexmedetomidine-inhibited chronic inflammatory visceral pain by targeting to HDAC2

Chaperone co-inducer BGP-15 inhibits histone deacetylases and enhances the heat shock response through increased chromatin accessibility

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