Tanshinone IIA Exerts an Antinociceptive Effect
in Rats with Cancer-induced Bone Pain

Background: Cancer-induced bone pain (CIBP) is a common chronic pain characterized by 2 components, ongoing pain and breakthrough pain. Tanshinone IIA (TSN IIA) is a bioactive constituent of the traditional Chinese medicine Danshen, which has been reported to have an antinociceptive effect on neuropathic and inflammatory pain through downregulation of the late proinflammatory cytokine high-mobility group protein B1 (HMGB1). Objective: To assess the antinociceptive effect of TSN IIA on CIBP. Study Design: A randomized, double-blind, controlled animal trial was performed. Setting: University lab in China. Methods: A rat CIBP model was established by injecting Walker 256 mammary gland carcinoma cells into the intramedullary cavity of the tibia. Both ongoing pain, e.g., flinching and guarding, and breakthrough pain, e.g., limb use and von Frey threshold, were evaluated. The effects of intraperitoneally administered TSN IIA on pain behavior and the expression levels of spinal HMGB1, interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6 were determined. The effect of TSN IIA on the electrically evoked response of spinal wide-dynamic range (WDR) neurons was performed in vivo. Results: TSN IIA dose-dependently inhibited cancer-induced ongoing pain and breakthrough pain. The expression levels of spinal HMGB1 and other inflammatory factors (IL-1β, TNF-α, and IL-6) were increased in the rat model, but they were suppressed by TSN IIA in a dose-dependent manner. Moreover, TSN IIA significantly inhibited the neuronal responses of WDR neurons in spinal deep layers. Limitations: Further studies are warranted to ascertain how TSN IIA attenuates cancer-induced ongoing pain. Conclusions: Our results indicate that TSN IIA attenuates cancer-induced ongoing pain and breakthrough pain, possibly via suppression of central sensitization in CIBP rats. Therefore, we have provided strong evidence supporting TSN IIA as a potential and effective therapy for relieving CIBP. Key words: Cancer-induced bone pain, high-mobility group protein B1, Tanshinone IIA, ongoing pain, breakthrough pain

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High Mobility Group Protein HMG-R

10.32388/nb6yys ◽

2020 ◽

Author(s):

Keyword(s):

High Mobility ◽

High Mobility Group ◽

High Mobility Group Protein ◽

Group Protein

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Faculty Opinions recommendation of Actively transcribed rRNA genes in S. cerevisiae are organized in a specialized chromatin associated with the high-mobility group protein Hmo1 and are largely devoid of histone molecules.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1144960.602064 ◽

2009 ◽

Author(s):

Jim Maher

Keyword(s):

High Mobility ◽

High Mobility Group ◽

Rrna Genes ◽

High Mobility Group Protein ◽

Group Protein

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HMGA1 Is a Potential Driver of Preeclampsia Pathogenesis by Interference with Extravillous Trophoblasts Invasion

Biomolecules ◽

10.3390/biom11060822 ◽

2021 ◽

Vol 11 (6) ◽

pp. 822

Author(s):

Keiichi Matsubara ◽

Yuko Matsubara ◽

Yuka Uchikura ◽

Katsuko Takagi ◽

Akiko Yano ◽

...

Keyword(s):

Protein A ◽

High Mobility ◽

Extravillous Trophoblast ◽

High Mobility Group Protein ◽

Successful Pregnancy ◽

Group Protein ◽

Serious Disease ◽

Proliferation And Invasion ◽

Extravillous Trophoblasts ◽

Fertilized Egg

Preeclampsia (PE) is a serious disease that can be fatal for the mother and fetus. The two-stage theory has been proposed as its cause, with the first stage comprising poor placentation associated with the failure of fertilized egg implantation. Successful implantation and placentation require maternal immunotolerance of the fertilized egg as a semi-allograft and appropriate extravillous trophoblast (EVT) invasion of the decidua and myometrium. The disturbance of EVT invasion during implantation in PE results in impaired spiral artery remodeling. PE is thought to be caused by hypoxia during remodeling failure–derived poor placentation, which results in chronic inflammation. High-mobility group protein A (HMGA) is involved in the growth and invasion of cancer cells and likely in the growth and invasion of trophoblasts. Its mechanism of action is associated with immunotolerance. Thus, HMGA is thought to play a pivotal role in successful pregnancy, and its dysfunction may be related to the pathogenesis of PE. The evaluation of HMGA function and its changes in PE might confirm that it is a reliable biomarker of PE and provide prospects for PE treatment through the induction of EVT proliferation and invasion during the implantation.

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