OBJECTIVETo investigate whether formalin inflammatory pain can induce the change in heme oxygenase-1 (HO-1) expression in the spinal cord of rats or not and the time course character.

METHODS42 SD rats were divided into 7 groups (n = 6): control formalin 6 h, formalin 12 h, formalin 1 d, formalin 2 d, formalin 3 d and formalin 7 d groups. Rats were subcutaneously injected with 0.2 ml 0.5% formalin into the ventral surface of right hind paw to induce periphery inflammatory pain. The immunohistochemistry was used to observe the expression of HO-1 protein in laminae I - II of the spinal cord dorsal horn and the area around canalis centralis of the I5 spinal segment of rats.

RESULTSThere are rare HO-1 immunoreactive cells in the laminae I - II of the dorsal horn and the area around canalis centralis of the I5 spinal segment of rats of control group and HO-1 immunoreactive cells were light in staining degree. Comparing with control group, the numbers of HO-1 immunoreactive cells in the I - II laminae of dorsal horn and area around canalis centralis were increased in the rats at 6 h after formalin injection. The number and staining degree of HO-1 immunoreactive cells were further increased at 12 h and peaked at 1 d after formalin injection. They didn't return to normal level at the 7th day. There were no difference in right and left dorsal horn in the number and staining degree of HO-1 immunoreactive cells at the same time after formalin injection.

CONCLUSIONFormalin inflammatory pain induced increased expression of HO-1 in the spinal cord dorsal horn and the area around canalis centralis of rats. At 1 d after injection of formalin, the increased expression of HO-1 was the most obviously.

Animals ; Formaldehyde ; adverse effects ; Heme Oxygenase (Decyclizing) ; metabolism ; Male ; Pain ; metabolism ; Pain Measurement ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism

OBJECTIVETo probe into the best parameter of electroacupuncture (EA) for treatment of inflammatory pain in the rat.

METHODSOne hundred and twenty Wistar rats were randomly divided into 12 groups, normal control group, model group and 10 EA groups including A1 B1 C1, A1 B1 C2, A1 B2 C1, A1 B2 C2, A2 B1 C1, A2 B1 C2, A2 B2 C1, A2 B2 C2 (A1 : 2 Hz, A2: 100 Hz; B1 : successive wave; B2: intermittent wave; C1: 0.1 mA, C2: 0.2 mA), A3 B3 C1 (4/20 Hz, disperse-dense wave, 0.1 mA) and A3 B3 C2 (4/20 Hz, disperse-dense wave, 0.2 mA). The rats of adjuvant-induced arthritis in all of the EA groups were treated by EA with selected different parameters once every day for 6 days. Pain thresholds and beta-endorphin (beta-EP) content in the local tissue of inflammation were used as indexes to compare analgesic effects of EA of different frequencies, waveforms and currents by orthogonal experiment design and other methods.

RESULTSThe optimized parameters of raising the pain threshold was: 100 Hz, 0.1 mA, intermittent wave. EA at 100 Hz was better than 2 Hz for increasing the content of beta-EP in local tissue of inflammation. The analgesic effect of EA at 4/20 Hz, 0.1 mA, disperse-dense wave on the inflammatory pain in the rat was not significant different with that at 100 Hz, 0.1 mA, intermittent wave (P > 0.05).

CONCLUSIONThe best parameters are 100 Hz, 0.1 mA and intermittent wave for EA treatment of inflammatory pain in the rat.

Acupuncture Analgesia ; Animals ; Arthritis ; metabolism ; physiopathology ; therapy ; Electroacupuncture ; Female ; Humans ; Pain ; metabolism ; physiopathology ; Pain Management ; Pain Threshold ; Random Allocation ; Rats ; Rats, Wistar ; beta-Endorphin ; metabolism

Amino Acids ; metabolism ; Animals ; Brain ; metabolism ; Electromagnetic Fields ; Electrophysiological Phenomena ; Glutamates ; metabolism ; Male ; Neurotransmitter Agents ; metabolism ; Pain ; physiopathology ; Pain Threshold ; Rats ; Rats, Sprague-Dawley ; gamma-Aminobutyric Acid ; metabolism

Nociception is an important physiological process that detects harmful signals and results in pain perception. In this review, we discuss important experimental evidence involving some TRP ion channels as molecular sensors of chemical, thermal, and mechanical noxious stimuli to evoke the pain and itch sensations. Among them are the TRPA1 channel, members of the vanilloid subfamily (TRPV1, TRPV3, and TRPV4), and finally members of the melastatin group (TRPM2, TRPM3, and TRPM8). Given that pain and itch are pro-survival, evolutionarily-honed protective mechanisms, care has to be exercised when developing inhibitory/modulatory compounds targeting specific pain/itch-TRPs so that physiological protective mechanisms are not disabled to a degree that stimulus-mediated injury can occur. Such events have impeded the development of safe and effective TRPV1-modulating compounds and have diverted substantial resources. A beneficial outcome can be readily accomplished via simple dosing strategies, and also by incorporating medicinal chemistry design features during compound design and synthesis. Beyond clinical use, where compounds that target more than one channel might have a place and possibly have advantageous features, highly specific and high-potency compounds will be helpful in mechanistic discovery at the structure-function level.
Animals ; Humans ; Pain ; metabolism ; Pruritus ; metabolism ; Transient Receptor Potential Channels ; metabolism

OBJECTIVETo examine the effect of acute incisional pain on the expression of connexin 43 in rat spinal cord dorsal horn.

METHODSEighty rats were assigned into control group without any treatment and incisional pain group with incision surgery. For paw incisions, a 1-cm longitudinal incision was made through the skin and fascia of the plantar aspect of the right hind paw. After surgery, the 50% paw withdrawal threshold (PWT) was assessed in response to a tactile stimulus with calibrated von Frey monofilaments at 1, 2, 4 and 24 h, respectively. The spinal cord dorsal horn of rats was isolated at 1, 2, and 4 h after the surgery to assess the expression of connexin 43 using Western blotting and immunofluorescence assay.

RESULTSThe 50% PWT of the rats was significantly decreased after the incision surgery, and this decrement was the most obvious at 2 and 4 h. Western blotting and immunofluorescence assay showed that the expression of connexin 43 in the spinal cord dorsal horn was significantly increased in rats receiving the surgery especially at 2 and 4 h after the surgery.

CONCLUSIONIncision surgery induces an significant increase in connexin 43 expression in rat spinal cord dorsal horn, suggestting an potential role of connexin43 in postoperative incisional pain.

Animals ; Connexin 43 ; metabolism ; Pain, Postoperative ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Dorsal Horn ; metabolism

Acupuncture Analgesia ; Animals ; Humans ; Meridians ; Pain ; immunology ; metabolism ; Pain Management ; Signal Transduction

OBJECTIVETo investigate the current practice of myofascial pain syndrome (MPS) including current epidemiology, pathology, diagnosis and treatment.

DATA SOURCESThe data analyzed in this review were mainly from relevant articles without restriction on the publication date reported in PubMed, MedSci, Google scholar. The terms "myofasial trigger points" and "myofacial pain syndrome" were used for the literature search.

STUDY SELECTIONOriginal articles with no limitation of research design and critical reviews containing data relevant to myofascial trigger points (MTrPs) and MPS were retrieved, reviewed, analyzed and summarized.

RESULTSMyofascial pain syndrome (MPS) is characterized by painful taut band, referred pain, and local response twitch with a prevalence of 85% to 95% of incidence. Several factors link to the etiology of MTrPs, such as the chronic injury and overload of muscles. Other factors, such as certain nutrient and hormone insufficiency, comorbidities, and muscle imbalance may also maintain the MTrP in an active status and induce recurrent pain. The current pathology is that an extra leakage acetylcholine at the neuromuscular junction induces persistent contracture knots, relative to some hypotheses of integration, muscle spindle discharges, spinal segment sensitization, ect. MTrPs can be diagnosed and localized based on a few subjective criteria. Several approaches, including both direct and supplementary treatments, can inactivate MTrPs. Direct treatments are categorized into invasive and conservative.

CONCLUSIONThis review provides a clear understanding of MTrP pain and introduces the most useful treatment approaches in China.

China ; Humans ; Myofascial Pain Syndromes ; metabolism ; physiopathology ; Trigger Points ; physiology

Humans ; Sodium-Calcium Exchanger ; Carrier Proteins ; Pain ; Calcium/metabolism*

OBJECTIVE: To explore the role of phosphorylation of cAMP response element binding protein (CREB) in the incision-induced pain hypersensitivity. METHODS: A longitudinal incision was made in one plantar hind paw of isoflurane-anesthetized rats. Spinal cords were removed at various postoperative time after behavior test. Phosphorylation of CREB was determined by immunohistochemistry and double-labeling immunofluorescence. Morphine and gabapentin were intraperitoneally injected before the behavior test and were used to determine the interaction between phosphorylation of CREB and morphine and gabapentin. RESULTS: After the hind-paw incision, phosphorylation of CREB was enhanced in the ipsilateral lumbar spinal cord (P<0.05). The enhancement of p-CREB was mainly in the neurons in the dorsal horn of the spinal cord. All these were shown by double-labeling technique and p-CREB was mainly in the neurons. Intraperitoneal injection of morphine prevented the increased phosphorylation of CREB in the spinal cord and inhibited the mechanical allodynia induced by the incision (P>0.05). Gabapentin didn't inhibit the phosphorylation of CREB (P<0.05) but partly inhibited the mechanical allodynia. CONCLUSION Incision induces the phosphorylation of CREB in the spinal cord, and the increase of p-CREB is mainly in the neurons. Phosphorylation of CREB in the spinal cord contributes to the pain hypersensitivity induced by surgical incision.
Animals ; Cyclic AMP Response Element-Binding Protein ; metabolism ; Female ; Foot ; surgery ; Neurons ; metabolism ; Pain Threshold ; Pain, Postoperative ; metabolism ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism

We investigated the therapeutic effects of superoxide dismutase (SOD) from thermophilic bacterium HB27 on chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and its underlying mechanisms. A Sprague-Dawley rat model of CP/CPPS was prepared and then administered saline or Thermus thermophilic (Tt)-SOD intragastrically for 4 weeks. Prostate inflammation and fibrosis were analyzed by hematoxylin and eosin staining, and Masson staining. Alanine transaminase (ALT), aspartate transaminase (AST), serum creatinine (CR), and blood urea nitrogen (BUN) levels were assayed for all animals. Enzyme-linked immunosorbent assays (ELISA) were performed to analyze serum cytokine concentrations and tissue levels of malondialdehyde, nitric oxide, SOD, catalase, and glutathione peroxidase. Reactive oxygen species levels were detected using dichlorofluorescein diacetate. The messenger ribonucleic acid (mRNA) expression of tissue cytokines was analyzed by reverse transcription polymerase chain reaction (RT-PCR), and infiltrating inflammatory cells were examined using immunohistochemistry. Nuclear factor-κB (NF-κB) P65, P38, and inhibitor of nuclear factor-κBα (I-κBα) protein levels were determined using western blot. Tt-SOD significantly improved histopathological changes in CP/CPPS, reduced inflammatory cell infiltration and fibrosis, increased pain threshold, and reduced the prostate index. Tt-SOD treatment showed no significant effect on ALT, AST, CR, or BUN levels. Furthermore, Tt-SOD reduced inflammatory cytokine expression in prostate tissue and increased antioxidant capacity. This anti-inflammatory activity correlated with decreases in the abundance of cluster of differentiation 3 (CD3), cluster of differentiation 45 (CD45), and macrophage inflammatory protein 1α (MIP1α) cells. Tt-SOD alleviated inflammation and oxidative stress by reducing NF-κB P65 and P38 protein levels and increasing I-κBα protein levels. These findings support Tt-SOD as a potential drug for CP/CPPS.
Animals ; Chronic Pain ; Cytokines/metabolism* ; Fibrosis ; Humans ; Inflammation/metabolism* ; Male ; NF-kappa B/metabolism* ; Pelvic Pain/pathology* ; Prostatitis/metabolism* ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; Syndrome