Role of Transient Receptor Potential Vanilloid 1 in Electroacupuncture Analgesia on Chronic Inflammatory Pain in Mice

Yang, Jun; Hsieh, Ching Liang; Lin, Yi Wen

doi:10.1155/2017/5068347

Cited by 23 publications

(26 citation statements)

References 41 publications

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“…Consistent with results reported previously,36,37 we found that the CCI injury upregulated the expression of PKC and PKA, it also elevated the value of p-PKC/PKC and p-PKA/PKA in the DRGs of rats. However, TRPM8 blocking can only reduce p-PKC/PKC but not p-PKA/PKA; hence, it is reasonable to consider that PKC (not PKA) signaling is involved in the TRPM8-regulated hyperalgesia induced by nerve injury although PKA involved the neuropathic pain event.…”

Section: Discussionsupporting

confidence: 93%

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-κB signaling in the dorsal root ganglion of rats with neuropathic pain</p>

Cao

Hou

et al. 2019

JPR

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Background: TRPM8 channel plays central roles in the sensitization of nociceptive transduction and is thought as one of the potential targets for the treatment of neuropathic pain. However, the specific molecular mechanisms are still less clear. Methods: Sciatic chronic constriction injury (CCI) rats were intrathecally administered with AMTB (TRPM8-selective antagonist) or PDTC (nuclear factor-kappa B (NF-κB) inhibitor). Cold-, thermal- and mechanical-pain thresholds were examined in CCI and sham-operated rats before and after intrathecal administration of AMTB or PDTC. Protein expression levels of TRPM8 and NF-κB p65, p-PKC/PKC value and p-PKA/PKA value in the CCI ipsilateral L4-6 dorsal root ganglions (DRGs) were analyzed. In addition, the co-expression of TRPM8 and NF-κB was evaluated in DRG. Results: Intrathecal injection of AMTB decreased the cold hypersensitivity and aggravated the thermal-hyperalgesia in the next 2 weeks after CCI surgery. The protein expression of TRPM8 and NF-κB p65 in the ipsilateral DRGs significantly increased after CCI surgery, which can be reversed by intrathecal administration of AMTB. The PKC, PKA, p-PKC/PKC and p-PKA/PKA values showed significantly increase after CCI surgery, while intrathecal AMTB administration offset the expression increase of PKC, p-PKC and p-PKC/PKC but PKA or p-PKA/PKA in the DRG. NF-κB inhibitor not only efficiently increased the cold-, thermal-pain threshold of CCI rats, but also enhanced AMTB’s anti-cold pain effect although exerted no anti-thermal hyperalgesia effect compared with TRPM8 blockade group. Immunofluorescence results showed co-expression of TRPM8 and NF-κB in DRG neurons. Conclusion: TRPM8 channels in DRGs participate in the pathogenesis of cold and thermal hyperalgesia (not mechanical allodynia) in rats with neuropathic pain, which could be regulated by PKC (not PKA) and NF-κB signaling. TRPM8 channel, PKC and NF-κB are potential targets for cold hyperalgesia treatment in neuropathic pain patients.

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Section: Discussionsupporting

confidence: 93%

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-κB signaling in the dorsal root ganglion of rats with neuropathic pain</p>

Cao

Hou

et al. 2019

JPR

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“…Here, we scrutinized our CP/CPPS mouse model at day 20 and demonstrated that the absence of TRPV1 disrupts the development of pelvic tactile allodynia in mice with EAP (Figure A and B). Hence, our results align with other pain studies that showed a blunted pain response in TRPV1 KO mice . Then, we assessed whether inflammation is diminished in TRPV1 deficient tissue; as reported by several studies .…”

Section: Discussionsupporting

confidence: 87%

“…Hence, our results align with other pain studies that showed a blunted pain response in TRPV1 KO mice. 27,51,52 Then, we assessed whether inflammation is diminished in TRPV1 deficient tissue; as reported by several studies. 53,54 Our data revealed that global deletion of the TRPV1 channel did not quench prostate inflammation after the induction of EAP at day 20 ( Figure 2C and 2D).…”

Section: Trpv1 Antagonist Blunts Persistent Pelvic Tactile Allodyniamentioning

confidence: 99%

TRPV1 in experimental autoimmune prostatitis

et al. 2019

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Background Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a disorder that is characterized by persistent pelvic pain in men of any age. Although several studies suggest that the transient receptor potential vanilloid 1 (TRPV1) channel is involved in various pathways of chronic pain, the TRPV1 channel has not been implicated in chronic pelvic pain associated with CP/CPPS. Methods Male C57BL/6J (B6) and TRPV1 knockout (TRPV1 KO) mice (5‐7 weeks old) were used to study the development of pelvic allodynia in a murine model of CP/CPPS called experimental autoimmune prostatitis (EAP). The prostate lobes, dorsal root ganglia (DRG), and spinal cord were excised at day 20. The prostate lobes were assessed for inflammation, TRPV1 expression, and mast cell activity. DRG and spinal cord, between the L6‐S4 regions, were analyzed to determine the levels of phosphorylated ERK1/2 (p‐ERK 1/2). To examine the therapeutic potential of TRPV1, B6 mice with EAP received intraurethral infusion of a TRPV1 antagonist at day 20 (repeated every 2 days) and pelvic pain was evaluated at days 20, 25, 30, and 35. Results Our data showed that B6 mice with EAP developed pelvic tactile allodynia at days 7, 14, and 20. In contrast, TRPV1 KO mice with EAP do not develop pelvic tactile allodynia at any time point. Although we observed no change in the levels of TRPV1 protein expression in the prostate from B6 mice with EAP, there was evidence of significant inflammation and elevated mast cell activation. Interestingly, the prostate from TRPV1 KO mice with EAP showed a lack of mast cell activation despite evidence of prostate inflammation. Next, we observed a significant increase of p‐ERK1/2 in the DRG and spinal cord from B6 mice with EAP; however, p‐ERK1/2 expression was unaltered in TRPV1 KO mice with EAP. Finally, we confirmed that intraurethral administration of a TRPV1 antagonist peptide reduced pelvic tactile allodynia in B6 mice with EAP after day 20. Conclusions We demonstrated that in a murine model of CP/CPPS, the TRPV1 channel is key to persistent pelvic tactile allodynia and blocking TRPV1 in the prostate may be a promising strategy to quell chronic pelvic pain.

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“…Pain research on animals showed that acupuncture could suppress inflammation and reduce the levels of reactive oxidative species. For example, in a mouse model of chronic inflammatory pain, electroacupuncture modulated the inflammatory mediators such as glial fibrillary acidic protein (GFAP) and the receptor of advanced glycation end products (RAGE) [99]. Collectively, acupuncture seems to be able to promote postoperative recovery through an array of mechanisms.…”

Section: Reducing the Use Of Anesthetic Agents Promoting Patientmentioning

confidence: 99%

Application of Acupuncture to Attenuate Immune Responses and Oxidative Stress in Postoperative Cognitive Dysfunction: What Do We Know So Far?

Zhao

Yeung

et al. 2020

Oxidative Medicine and Cellular Longevity

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Postoperative cognitive dysfunction (POCD) is a common sequela following surgery and hospitalization. The prevention and management of POCD are important during clinical practice. POCD more commonly affects elderly patients who have undergone major surgery and can result in major decline in quality of life for both patients and their families. Acupuncture has been suggested as an effective intervention for many neurological disorders. In recent years, there are increasing interest in the use of acupuncture to prevent and treat POCD. In this review, we summarized the clinical and preclinical evidence of acupuncture on POCD using a narrative approach and discussed the potential mechanisms involved. The experimental details and findings of studies were summarized in tables and analyzed. Most of the clinical studies suggested that acupuncture before surgery could reduce the incidence of POCD and reduce the levels of systematic inflammatory markers. However, their reliability is limited by methodological flaws. Animal studies showed that acupuncture reduced cognitive impairment and the associated pathology after various types of surgery. It is possible that acupuncture modulates inflammation, oxidative stress, synaptic changes, and other cellular events to mitigate POCD. In conclusion, acupuncture is a potential intervention for POCD. More clinical studies with good research design are required to confirm its effectiveness. At the same time, findings from animal studies will help reveal the protective mechanisms, in which systematic inflammation is likely to play a major role.

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Role of Transient Receptor Potential Vanilloid 1 in Electroacupuncture Analgesia on Chronic Inflammatory Pain in Mice

Cited by 23 publications

References 41 publications

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-κB signaling in the dorsal root ganglion of rats with neuropathic pain</p>

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-κB signaling in the dorsal root ganglion of rats with neuropathic pain</p>

TRPV1 in experimental autoimmune prostatitis

Application of Acupuncture to Attenuate Immune Responses and Oxidative Stress in Postoperative Cognitive Dysfunction: What Do We Know So Far?

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Role of Transient Receptor Potential Vanilloid 1 in Electroacupuncture Analgesia on Chronic Inflammatory Pain in Mice

Cited by 23 publications

References 41 publications

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-&kappa;B signaling in the dorsal root ganglion of rats with neuropathic pain</p>

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-&kappa;B signaling in the dorsal root ganglion of rats with neuropathic pain</p>

TRPV1 in experimental autoimmune prostatitis

Application of Acupuncture to Attenuate Immune Responses and Oxidative Stress in Postoperative Cognitive Dysfunction: What Do We Know So Far?

Contact Info

Product

Resources

About

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-κB signaling in the dorsal root ganglion of rats with neuropathic pain</p>

<p>Intrathecal TRPM8 blocking attenuates cold hyperalgesia via PKC and NF-κB signaling in the dorsal root ganglion of rats with neuropathic pain</p>