Mild Moxibustion Decreases the Expression of Prokineticin 2 and Prokineticin Receptor 2 in the Colon and Spinal Cord of Rats with Irritable Bowel Syndrome

Zhou, Cili; Zhao, Jimeng; Wu, Luyi; Huang, Renjia; Shi, Yin; Wang, Xiaomei; Liao, Wen Ling; Jun-hee, Hong.; Liu, Shimin; Wu, Huangan

doi:10.1155/2014/807308

Cited by 10 publications

(6 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The expression of PKR1 in the urothelium is upregulated after CYP treatment, as indicated by our IHC data, as a response to inflammatory stimulation ( Figure 2 ). Similar results were reported in studies on other tissues, including the epithelium, under physiological and/or pathological conditions [ 25 , 29 – 31 ]. CYP administration can cause immune cells to infiltrate into the bladder wall, suggesting that the immigrating and activated immune cells possibly contribute to the overexpression of PKR1 in cystitis as PKR1 is expressed on these cells.…”

Section: Discussionsupporting

confidence: 90%

PK2/PKR1 Signaling Regulates Bladder Function and Sensation in Rats with Cyclophosphamide‐Induced Cystitis

Chen

Zhang

Liu

et al. 2015

Mediators of Inflammation

View full text Add to dashboard Cite

Prokineticin 2 (PK2) is a novel chemokine-like peptide with multiple proinflammatory and nociception-related activities. This study aimed to explore the potential role of PK2 in modulating bladder activity and sensation in rats with cyclophosphamide- (CYP-) induced cystitis. Changes of PK2 and prokineticin receptors (PKRs) in normal and inflamed urinary bladders were determined at several time points (4 h, 48 h, and 8 d) after CYP treatment. Combining a nonselective antagonist of prokineticin receptors (PKRA), we further evaluated the regulatory role of PK2 in modulating bladder function and visceral pain sensation via conscious cystometry and pain behavioral scoring. PK2 and prokineticin receptor 1 (PKR1), but not prokineticin receptor 2, were detected in normal and upregulated in CYP-treated rat bladders at several levels. Immunohistochemistry staining localized PKR1 primarily in the urothelium. Blocking PKRs with PKRA showed no effect on micturition reflex activity and bladder sensation in control rats while it increased the voiding volume, prolonged voiding interval, and ameliorated visceral hyperalgesia in rats suffering from CYP-induced cystitis. In conclusion, PK2/PKR1 signaling pathway contributes to the modulation of inflammation-mediated voiding dysfunction and spontaneous visceral pain. Local blockade of PKRs may represent a novel and promising therapeutic strategy for the clinical management of inflammation-related bladder diseases.

show abstract

Section: Discussionsupporting

confidence: 90%

PK2/PKR1 Signaling Regulates Bladder Function and Sensation in Rats with Cyclophosphamide‐Induced Cystitis

Chen

Zhang

Liu

et al. 2015

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…It activates the PKs receptors in the spinal dorsal horn and astrocytes, thereby promoting central sensitization and maintaining chronic and neuropathic pain ( Negri and Maftei, 2018 ). Two studies on mild moxibustion revealed that ST25 can inhibit the protein and mRNA expression of PK1/Prokineticin receptor (PKR) 1 and PK2/PKR2 in the spinal cord of IBS rats, respectively ( Zhao et al, 2012 ; Zhou et al, 2014 ). These findings suggest that acupuncture may exert its effects by suppressing the activity of central glial cells by inhibiting P2X7 and PKs pathways in the spinal cord.…”

Section: Resultsmentioning

confidence: 99%

The efficacy and neural mechanism of acupuncture therapy in the treatment of visceral hypersensitivity in irritable bowel syndrome

Yang,

Wang,

Zhang

et al. 2023

Front. Neurosci.

View full text Add to dashboard Cite

Irritable Bowel Syndrome (IBS) is a complex functional gastrointestinal disorder primarily characterized by chronic abdominal pain, bloating, and altered bowel habits. Chronic abdominal pain caused by visceral Hypersensitivity (VH) is the main reason why patients with IBS seek medication. Significant research effort has been devoted to the efficacy of acupuncture as a non-drug alternative therapy for visceral-hyperalgesia-induced IBS. Herein, we examined the central and peripheral analgesic mechanisms of acupuncture in IBS treatment. Acupuncture can improve inflammation and relieve pain by reducing 5-hydroxytryptamine and 5-HT3A receptor expression and increasing 5-HT4 receptor expression in peripheral intestinal sensory endings. Moreover, acupuncture can also activate the transient receptor potential vanillin 1 channel, block the activity of intestinal glial cells, and reduce the secretion of local pain-related neurotransmitters, thereby weakening peripheral sensitization. Moreover, by inhibiting the activation of N-methyl-D-aspartate receptor ion channels in the dorsal horn of the spinal cord and anterior cingulate cortex or releasing opioids, acupuncture can block excessive stimulation of abnormal pain signals in the brain and spinal cord. It can also stimulate glial cells (through the P2X7 and prokinetic protein pathways) to block VH pain perception and cognition. Furthermore, acupuncture can regulate the emotional components of IBS by targeting hypothalamic-pituitary-adrenal axis-related hormones and neurotransmitters via relevant brain nuclei, hence improving the IBS-induced VH response. These findings provide a scientific basis for acupuncture as an effective clinical adjuvant therapy for IBS pain.

show abstract

“…This suggests that in intestinal inflammatory pathways PK1/PKR1 might be a possible trigger, promoting, in loco, the recruitment of immune cells and inducing pro-inflammatory cytokine production. Subsequently, the role of the PKS in visceral pain was also investigated by Wu's research group [52,103]. A model of visceral hypersensitivity induced via chronic and repetitive colorectal distension (CCD) in rats was used in both of these studies.…”

Section: Evidence Of the Pks In Pain: Focus On Ibd Modelmentioning

confidence: 99%

The Prokineticin System in Inflammatory Bowel Diseases: A Clinical and Preclinical Overview

Amodeo,

Franchi,

Galimberti

et al. 2023

Biomedicines

View full text Add to dashboard Cite

Inflammatory bowel disease (IBD) includes Crohn’s disease (CD) and ulcerative colitis (UC), which are characterized by chronic inflammation of the gastrointestinal (GI) tract. IBDs clinical manifestations are heterogeneous and characterized by a chronic relapsing-remitting course. Typical gastrointestinal signs and symptoms include diarrhea, GI bleeding, weight loss, and abdominal pain. Moreover, the presence of pain often manifests in the remitting disease phase. As a result, patients report a further reduction in life quality. Despite the scientific advances implemented in the last two decades and the therapies aimed at inducing or maintaining IBDs in a remissive condition, to date, their pathophysiology still remains unknown. In this scenario, the importance of identifying a common and effective therapeutic target for both digestive symptoms and pain remains a priority. Recent clinical and preclinical studies have reported the prokineticin system (PKS) as an emerging therapeutic target for IBDs. PKS alterations are likely to play a role in IBDs at multiple levels, such as in intestinal motility, local inflammation, ulceration processes, localized abdominal and visceral pain, as well as central nervous system sensitization, leading to the development of chronic and widespread pain. This narrative review summarized the evidence about the involvement of the PKS in IBD and discussed its potential as a druggable target.

show abstract

Mild Moxibustion Decreases the Expression of Prokineticin 2 and Prokineticin Receptor 2 in the Colon and Spinal Cord of Rats with Irritable Bowel Syndrome

Cited by 10 publications

References 40 publications

PK2/PKR1 Signaling Regulates Bladder Function and Sensation in Rats with Cyclophosphamide‐Induced Cystitis

PK2/PKR1 Signaling Regulates Bladder Function and Sensation in Rats with Cyclophosphamide‐Induced Cystitis

The efficacy and neural mechanism of acupuncture therapy in the treatment of visceral hypersensitivity in irritable bowel syndrome

The Prokineticin System in Inflammatory Bowel Diseases: A Clinical and Preclinical Overview

Contact Info

Product

Resources

About