Resveratrol reverses morphine-induced neuroinflammation in morphine-tolerant rats by reversal HDAC1 expression

Tsai, Ray Jui-Fang; Wang, Juei-Chii; Chou, Kuang-Yi; Wong, Chih‐Shung; Cherng, Chen‐Hwan

doi:10.1016/j.jfma.2015.05.010

Cited by 24 publications

(13 citation statements)

References 44 publications

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“…The effects of HDACi on morphine tolerance are controversial. Some studies have indicated that HDACi can enhance the analgesic effects of morphine and attenuate morphine tolerance ( Dobashi et al, 2010 ; Tsai et al, 2016 ; Hou et al, 2017 ; Liao et al, 2018 ). However, some studies have demonstrated that chronic morphine treatment with simultaneous SAHA treatment can enhance opioid-induced hyperalgesia ( Liang et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Histone Deacetylases Attenuates Morphine Tolerance and Restores MOR Expression in the DRG of BCP Rats

Zhou

Zhao

et al. 2018

Front. Pharmacol.

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The easily developed morphine tolerance in bone cancer pain (BCP) significantly hindered its clinical use. Increasing evidence suggests that histone deacetylases (HDACs) regulate analgesic tolerance subsequent to continuous opioid exposure. However, whether HDACs contribute to morphine tolerance in the pathogenesis of BCP is still unknown. In the current study, we explored the possible engagement of HDACs in morphine tolerance during the pathogenesis of BCP. After intra-tibia tumor cell inoculation (TCI), we found that the increased expression of HDACs was negatively correlated with the decreased expression of MOR in the DRG following TCI. The paw withdrawal threshold (PWT) and percentage maximum possible effects (MPEs) decreased rapidly in TCI rats when morphine was used alone. In contrast, the concomitant use of SAHA and morphine significantly elevated the PWT and MPEs of TCI rats compared to morphine alone. Additionally, we found that SAHA administration significantly elevated MOR expression in the DRG of TCI rats with or without morphine treatment. Moreover, the TCI-induced increase in the co-expression of MOR and HDAC1 in neurons was significantly decreased after SAHA administration. These results suggest that HDACs are correlated with the downregulation of MOR in the DRG during the pathogenesis of BCP. Inhibition of HDACs using SAHA can be used to attenuate morphine tolerance in BCP.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Histone Deacetylases Attenuates Morphine Tolerance and Restores MOR Expression in the DRG of BCP Rats

Zhou

Zhao

et al. 2018

Front. Pharmacol.

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“…Up-regulation of HDAC2 in neurons by HIV TAT was associated with down-regulation of CREB and CaMKIIa genes that are known to regulate neuronal activity, suggesting the possible role of HDAC in HIV-associated neurocognitive disorder (44). Previous studies by Tsai et al showed that morphine induced HDAC1 up-regulation in rat spinal cord dorsal horn, which contributed to neuro-inflammation and subsequent tolerance (45). Therefore, it will be interesting to investigate the detailed mechanisms by which HIV and opioids modulate HDAC activities, and future studies will also examine how abnormal HDAC activities regulate host response to opioids and HIV.…”

Section: Disscussionmentioning

confidence: 95%

Opioids Impair Intestinal Epithelial Repair in HIV-Infected Humanized Mice

et al. 2020

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Intestinal barrier dysfunction and subsequent microbial translocation play crucial roles in persistent immune activation leading to HIV disease progression. Opioid use is associated with worse outcome in HIV-infected patients. The exacerbated disease progression by opioids is mainly driven by excessive intestinal inflammation and increased gut permeability. The objective of this study is to investigate how opioids potentiate HIV disease progression by compromising intestinal barrier function and impairing intestinal epithelial self-repair mechanism. In the present study, abnormal intestinal morphology and reduced epithelial proliferation were observed in bone marrow-liver-thymus humanized mice and in HIV-infected patients who were exposed to opioids. In bone marrow-liver-thymus mice, HIV, and morphine independently, and additively induced gut dysbiosis, especially depletion of Lachnospiraceae, Ruminococcaceae, and Muribaculaceae. We also observed that the abundance of Lachnospiraceae, Ruminococcaceae, and Muribaculaceae negatively correlated with apoptosis of epithelial cells, and intestinal IL-6 levels. Previous studies have shown that these bacterial families play crucial roles in maintaining intestinal homeostasis because they include most short-chain fatty acid-producing members. Short-chain fatty acids have been shown to maintain stem cell populations and suppress inflammation in the gut by inhibiting histone deacetylases (HDAC). In addition, we demonstrate that morphine exposure inhibited growth of intestinal organoids derived from HIV transgenic mice by suppressing Notch signaling in an HDAC-dependent manner. These studies implicate an important role for HDAC in intestinal homeostasis and supports HDAC modulation as a therapeutic intervention in improving care of HIV patients, especially in opioid-abusing population.

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“…In tactile allodynia caused by SNL, intrathecal injection of resveratrol can reduce the activity and expression of NOS, and alleviate tactile allodynia in rats with NPP (Pérez-Severiano et al, 2008). In a study by Tsai et al (2016), intrathecal injection of resveratrol reversed the increase in histone deacetylase 1 (HDAC1), TNF-α, and TNF receptor 1 (TNFR1) expression induced by long-term morphine infusion, and restored the antinociceptive effect in morphine-tolerant rats. Proanthocyanidins (PAs) are polyphenols in plant foods that have many health benefits, including cancer prevention, cardiovascular protection, and diabetes prevention (Zhang et al, 2016).…”

Section: Natural Medicines and Their Extractsmentioning

confidence: 99%

“…The use of microglial inhibitors can reverse the expression of pro-inflammatory factors during morphine infusion. The expression of microglial surface markers Iba-1, purinergic receptors (P2X4R and P2X7R), and TLR4 increases with increasing levels of glial medium (Tsai et al, 2016;Bisht et al, 2018). Targeting microglial activation may have great research value for the treatment of NPP and the prevention of morphine tolerance.…”

Section: Microglial Activation: a Bridge Between Npp And Morphine Tolmentioning

confidence: 99%

Regulatory mechanisms and therapeutic potential of microglial inhibitors in neuropathic pain and morphine tolerance

Fan

Rong

et al. 2020

J. Zhejiang Univ. Sci. B

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Microglia are important cells involved in the regulation of neuropathic pain (NPP) and morphine tolerance. Information on their plasticity and polarity has been elucidated after determining their physiological structure, but there is still much to learn about the role of this type of cell in NPP and morphine tolerance. Microglia mediate multiple functions in health and disease by controlling damage in the central nervous system (CNS) and endogenous immune responses to disease. Microglial activation can result in altered opioid system activity, and NPP is characterized by resistance to morphine. Here we investigate the regulatory mechanisms of microglia and review the potential of microglial inhibitors for modulating NPP and morphine tolerance. Targeted inhibition of glial activation is a clinically promising approach to the treatment of NPP and the prevention of morphine tolerance. Finally, we suggest directions for future research on microglial inhibitors.

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Resveratrol reverses morphine-induced neuroinflammation in morphine-tolerant rats by reversal HDAC1 expression

Cited by 24 publications

References 44 publications

Inhibition of Histone Deacetylases Attenuates Morphine Tolerance and Restores MOR Expression in the DRG of BCP Rats

Inhibition of Histone Deacetylases Attenuates Morphine Tolerance and Restores MOR Expression in the DRG of BCP Rats

Opioids Impair Intestinal Epithelial Repair in HIV-Infected Humanized Mice

Regulatory mechanisms and therapeutic potential of microglial inhibitors in neuropathic pain and morphine tolerance

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