Effects of Electroacupuncture with Different Frequencies on the Glycoconjugate Alterations in Articular Cartilage in the Ankle Joints of Complete Freund's Adjuvant-injected Rats

2006 ◽  
Vol 34 (03) ◽  
pp. 417-426 ◽  
Author(s):  
In-Bum Park ◽  
Chang-Beohm Ahn ◽  
Byung-Tae Choi

The aim of this study was to investigate the effects of electroacupuncture (EA) on the glycoconjugate (GC) changes in articular cartilage in the ankle of an arthritic model. Arthritis was induced by an intraplantar injection of complete Freund's adjuvant (CFA) into the hindpaw of male Sprague-Dawley rats. Bilateral EA stimulation at 2 Hz, 15 Hz and 120 Hz was applied at those acupoints corresponding to Zusanli and Sanyinjiao in man, using needles for 3-day intervals for 30 days. To determine the presence of arthritis, paw edema was measured by a water displacement plethysmometer. Edema of the hindpaw induced by CFA-injection was strongly inhibited by EA stimulation throughout the experimental period. At 30 days after CFA-injection, GC changes of articular cartilage of the ankle joint were observed using conventional and lectin histochemistry. The CFA-injected rat revealed general reduction of staining abilities and lectin affinities for GC in comparison with normal rats. Significant reductions of neutral and acidic GC were observed in interterritorial matrix and chondrocyte capsules, respectively. All lectin affinities examined except DBA were also decreased in CFA-injected rats compared to normal ones. However, EA-treated rats, showed similar staining patterns and lectin affinities for GC as to normal ones, especially neutral GC in interterritorial matrix and sWGA and RCA-1 affinities in chondrocytes. It is concluded that EA in all frequencies examined, especially 2 Hz, can attenuate inflammatory edema in CFA-injected rats through alleviation of alterations of GC components in articular cartilage.

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Edina K. Cseh ◽  
Gábor Veres ◽  
Tamás Körtési ◽  
Helga Polyák ◽  
Nikolett Nánási ◽  
...  

Abstract Background The neurochemical background of the evolution of headache disorders, still remains partially undiscovered. Accordingly, our aim was to further explore the neurochemical profile of Complete Freund’s adjuvant (CFA)-induced orofacial pain, involving finding the shift point regarding small molecule neurotransmitter concentrations changes vs. that of the previously characterized headache-related neuropeptides. The investigated neurotransmitters consisted of glutamate, γ-aminobutyric acid, noradrenalin and serotonin. Furthermore, in light of its influence on glutamatergic neurotransmission, we measured the level of kynurenic acid (KYNA) and its precursors in the kynurenine (KYN) pathway (KP) of tryptophan metabolism. Methods The effect of CFA was evaluated in male Sprague Dawley rats. Animals were injected with CFA (1 mg/ml, 50 μl/animal) into the right whisker pad. We applied high-performance liquid chromatography to determine the concentrations of the above-mentioned compounds from the trigeminal nucleus caudalis (TNC) and somatosensory cortex (ssCX) of rats. Furthermore, we measured some of these metabolites from the cerebrospinal fluid and plasma as well. Afterwards, we carried out permutation t-tests as post hoc analysis for pairwise comparison. Results Our results demonstrated that 24 h after CFA treatment, the level of glutamate, KYNA and that of its precursor, KYN was still elevated in the TNC, all diminishing by 48 h. In the ssCX, significant concentration increases of KYNA and serotonin were found. Conclusion This is the first study assessing neurotransmitter changes in the TNC and ssCX following CFA treatment, confirming the dominant role of glutamate in early pain processing and a compensatory elevation of KYNA with anti-glutamatergic properties. Furthermore, the current findings draw attention to the limited time interval where medications can target the glutamatergic pathways.


2010 ◽  
Vol 112 (2) ◽  
pp. 418-431 ◽  
Author(s):  
Yasuko Taketa ◽  
Keiichi Niikura ◽  
Yasuhisa Kobayashi ◽  
Masaharu Furuya ◽  
Toshikazu Shimizu ◽  
...  

Background Dynorphin A in the spinal cord is considered to contribute to nociceptive stimuli. However, it has not yet been determined whether activation of the spinal dynorphinergic system under nociceptive stimuli plays a role in direct acceleration of the ascending nociceptive pathway. In this study, the authors investigated the role of spinal dynorphinergic transmission in ongoing brain activation under noxious stimuli in mice. Methods The changes in prodynorphin messenger RNA expression and dynorphin A (1-17)-like immunoreactivity in the mouse spinal cord were determined after the intraplantar injection of complete Freund's adjuvant in mice. The signal intensity in different brain regions after the intraplantar injection of complete Freund's adjuvant or intrathecal injection of dynorphin A (1-17) was measured by a pharmacological functional magnetic resonance imaging analysis. Results Complete Freund's adjuvant injection produced pain-associated behaviors and induced a dramatic increase in signal intensity in the mouse cingulate cortex, somatosensory cortex, insular cortex, and thalamic nuclei. These effects were not seen in prodynorphin knockout mice. Prodynorphin messenger RNA expression and dynorphin A (1-17)-like immunoreactivity on the ipsilateral side of the spinal cord were markedly increased in complete Freund's adjuvant-injected mice. Furthermore, intrathecal injection of dynorphin A (1-17) at relatively high doses caused pain-associated behaviors and a remarkable increase in the activities of the cingulate cortex, somatosensory cortex, insular cortex, and medial and lateral thalamic nuclei in mice. Conclusions These findings indicate that spinally released dynorphin A (1-17) by noxious stimuli leads to the direct activation of ascending pain transmission.


2020 ◽  
Author(s):  
Edina K Cseh ◽  
Gábor Veres ◽  
Tamás Körtési ◽  
Helga Polyák ◽  
Nikolett Nánási ◽  
...  

Abstract Background The neurochemical background of the evolution of headache disorders, still remains partially undiscovered. Accordingly, our aim was to further explore the neurochemical profile of Complete Freund’s adjuvant (CFA)-induced orofacial pain, involving finding the shift point regarding small molecule neurotransmitter concentrations changes vs. that of the previously characterized headache-related neuropeptides. The investigated neurotransmitters consisted of glutamate, γ-aminobutyric acid, noradrenalin and serotonin. Furthermore, in light of its influence on glutamatergic neurotransmission, we measured the level of kynurenic acid (KYNA) and its precursors in the kynurenine (KYN) pathway (KP) of tryptophan metabolism. Methods The effect of CFA was evaluated in male Sprague Dawley rats. Animals were injected with CFA (1 mg/ml, 50 µl/animal) into the right whisker pad. We applied high-performance liquid chromatography to determine the concentrations of the above-mentioned compounds from the trigeminal nucleus caudalis (TNC) and somatosensory cortex (ssCX) of rats. Furthermore, we measured some of these metabolites from the cerebrospinal fluid and plasma as well. Afterwards, we carried out permutation t-tests as post hoc analysis for pairwise comparison. Results Our results demonstrated that 24 h after CFA treatment, the level of glutamate, KYNA and that of its precursor, KYN was still elevated in the TNC, all diminishing by 48 h. In the ssCX, significant concentration increases of KYNA and serotonin were found. Conclusion This is the first study assessing neurotransmitter changes in the TNC and ssCX following CFA treatment, confirming the dominant role of glutamate in early pain processing and a compensatory elevation of KYNA with anti-glutamatergic properties. Furthermore, the current findings draw attention to the limited time interval where medications can target the glutamatergic pathways.


2020 ◽  
Vol 19 (9) ◽  
pp. 1933-1939
Author(s):  
Yi Fan ◽  
Cheng Zhang ◽  
Guotao Zheng ◽  
Shuai Wu ◽  
Yujie Wang ◽  
...  

Purpose: To determine the anti-arthritic effect of arjunolic acid against complete Freund’s adjuvant (CFA)-induced arthritis in rats.Methods: Arthritis was induced in male Sprague Dawley rats by intradermal injection of 0.1 mL of CFA at the right footpad. Upon induction of osteoarthritis, arjunolic acid was administered via oral gavage at doses of 40 and 80 mg/kg once daily for 25 successive days. Indomethacin was used as reference drug at a dose of 3 mg/kg via gavage twice weekly for 25 days. Changes in paw swelling, serum hematology, antioxidant enzymes, serum inflammatory mediators, and histopathology were determined using standard procedures.Results: Paw swelling and weight loss in CFA-induced arthritic rats were significantly reversed (p < 0.01) by arjunolic acid. Malondialdehyde (MDA) levels, spleen index and thymus index were significantly reduced in CFA-induced arthritic rats (p < 0.01). Moreover, arjunolic significantly increased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, while downregulating the expressions of TNF-α, IL-1β and IL-6 in serum (p < 0.01). The hematological and histopathological changes due to CFA-induced arthritis were ameliorated by arjunolic acid.Conclusion: The results obtained in this study indicate that arjunolic acid may possess therapeutic potentials for the management of arthritis. Keywords: Arjunolic acid, Triterpenoid; Oxidative stress, osteoarthritis, Inflammation


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Yi Liang ◽  
Jian-Qiao Fang ◽  
Jun-Ying Du ◽  
Jun-Fan Fang

Activation of mitogen-activated protein kinases (MAPKs), especially p38 MAPK, plays an important role in the development of central sensitization related to persistent inflammatory pain. Electroacupuncture (EA) is well known to relieve persistent inflammatory pain. However, little is known about relationship between EA and p38 MAPK. Inflammatory pain rat model was induced by intraplantar injection of complete Freund's adjuvant (CFA). Male adult SD rats were randomly divided into the saline group, CFA group, and CFA + EA group. EA (constant saquare wave, 2 Hz and 100 Hz alternating frequencies, intensities ranging from 1 to 2 mA) was applied to bilateral “Zusanli” (ST 36) and “Kunlun” acupoints (BL 60) for 30 min, once per day. The paw edema and paw withdrawal threshold (PWT) were measured at preinjection and days postinjection 1, 3, and 14. Spinal p-p38MAPK- immunoreactivty (p-p38MAPK-IR) cells were detected by immunohistochemistry at postinjection day 3 and 14. EA significantly inhibited paw edema at postinjection days 14 and increased PWT at postinjection days 3 and 14. Moreover, the increasing number of spinal p-p38MAPK-IR cells which was induced by CFA injection was suppressed by EA stimulation. These results indicate that anti-inflammatory and analgesic effect of EA might be associated with its inhibition of spinal p38 MAPK activation and thereby provide a potential mechanism for the treatment of inflammatory pain by EA.


2014 ◽  
Vol 2014 ◽  
pp. 1-7
Author(s):  
Si-Ping Hu ◽  
Jing-Jing Zhao ◽  
Wei-Xing Wang ◽  
Yang Liu ◽  
He-Fen Wu ◽  
...  

The present study was aimed at investigating the analgesic properties of a combination of lidocaine and QX-222 and its effects on evoked pain behavior (complete Freund’s adjuvant-induced allodynia and hyperalgesia in inflammatory condition) and spontaneous pain behavior (formalin-induced acute pain) in mice. Drugs were injected adjacent to sciatic nerve or into plantar. Motor function, thermal withdrawal latency, mechanical withdrawal threshold, and licking/biting were evaluated by behavioral tests. A combination of lidocaine and QX-222 adjacent sciatic nerve injection produced the long-lasting sensory-specific nerve block, and intraplantar injection inhibited spontaneous pain in the formalin-treated mice but did not detectably attenuated hyperalgesia and allodynia in the complete Freund’s adjuvant- (CFA-) treated mice. Our results suggest that a combination of lidocaine and QX-222 achieves a long-lasting differential block (sensory selective) and produces divergent effects on evoked and spontaneous pain behaviors in mice.


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