-
Je něco špatně v tomto záznamu ?
Electroacupuncture inhibits the interaction between peripheral TRPV1 and P2X3 in rats with different pathological pain
Y. Liu, J. Du, J. Fang, X. Xiang, Y. Xu, S. Wang, H. Sun, J. Fang
Jazyk angličtina Země Česko
Typ dokumentu srovnávací studie, časopisecké články
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
PubMed Central
od 2020
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- elektroakupunktura * MeSH
- hyperalgezie metabolismus patofyziologie terapie MeSH
- kationtové kanály TRPV metabolismus MeSH
- modely nemocí na zvířatech MeSH
- neuralgie metabolismus patofyziologie terapie MeSH
- potkani Sprague-Dawley MeSH
- práh bolesti MeSH
- purinergní receptory P2X3 metabolismus MeSH
- signální transdukce MeSH
- spinální ganglia metabolismus patofyziologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- srovnávací studie MeSH
Chronic pain is regarded to be one of the common and refractory diseases to cure in the clinic. One hundred Hz electroacupuncture (EA) is commonly used for inflammatory pain and 2 Hz for neuropathic pain possibly by modulating the transient receptor potential vanilloid subtype 1 (TRPV1) or the purinergic P2X3 related pathways. To clarify the mechanism of EA under various conditions of pathological pain, rats received a subcutaneous administration of complete Freund's adjuvant (CFA) for inflammatory pain and spared nerve injury (SNI) for neuropathic pain. The EA was performed at the bilateral ST36 and BL60 1 d after CFA or SNI being successfully established for 3 consecutive days. The mechanical hyperalgesia test was measured at baseline, 1 d after model establishment, 1 d and 3 d after EA. The co-expression changes, co-immunoprecipitation of TRPV1 and P2X3, and spontaneous pain behaviors (SPB) test were performed 3 d after EA stimulation. One hundred Hz EA or 2Hz EA stimulation could effectively down-regulate the hyperalgesia of CFA or SNI rats. The increased co-expression ratio between TRPV1 and P2X3 at the dorsal root ganglion (DRG) in two types of pain could be reduced by 100Hz or 2Hz EA intervention. While 100Hz or 2Hz EA was not able to eliminate the direct physical interaction between TRPV1 and P2X3. Moreover, EA could significantly inhibit the SPB induced by the co-activation of peripheral TRPV1 and P2X3. All results indicated that EA could significantly reduce the hyperalgesia and the SPB, which was partly related to inhibiting the co-expression and indirect interaction between peripheral TRPV1 and P2X3.
Citace poskytuje Crossref.org
Literatura
- 000
- 00000naa a2200000 a 4500
- 001
- bmc22007906
- 003
- CZ-PrNML
- 005
- 20220323102117.0
- 007
- ta
- 008
- 220309s2021 xr d f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.934649 $2 doi
- 035 __
- $a (PubMed)34062076
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Liu, Yingjun $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 245 10
- $a Electroacupuncture inhibits the interaction between peripheral TRPV1 and P2X3 in rats with different pathological pain / $c Y. Liu, J. Du, J. Fang, X. Xiang, Y. Xu, S. Wang, H. Sun, J. Fang
- 504 __
- $a Literatura
- 520 9_
- $a Chronic pain is regarded to be one of the common and refractory diseases to cure in the clinic. One hundred Hz electroacupuncture (EA) is commonly used for inflammatory pain and 2 Hz for neuropathic pain possibly by modulating the transient receptor potential vanilloid subtype 1 (TRPV1) or the purinergic P2X3 related pathways. To clarify the mechanism of EA under various conditions of pathological pain, rats received a subcutaneous administration of complete Freund's adjuvant (CFA) for inflammatory pain and spared nerve injury (SNI) for neuropathic pain. The EA was performed at the bilateral ST36 and BL60 1 d after CFA or SNI being successfully established for 3 consecutive days. The mechanical hyperalgesia test was measured at baseline, 1 d after model establishment, 1 d and 3 d after EA. The co-expression changes, co-immunoprecipitation of TRPV1 and P2X3, and spontaneous pain behaviors (SPB) test were performed 3 d after EA stimulation. One hundred Hz EA or 2Hz EA stimulation could effectively down-regulate the hyperalgesia of CFA or SNI rats. The increased co-expression ratio between TRPV1 and P2X3 at the dorsal root ganglion (DRG) in two types of pain could be reduced by 100Hz or 2Hz EA intervention. While 100Hz or 2Hz EA was not able to eliminate the direct physical interaction between TRPV1 and P2X3. Moreover, EA could significantly inhibit the SPB induced by the co-activation of peripheral TRPV1 and P2X3. All results indicated that EA could significantly reduce the hyperalgesia and the SPB, which was partly related to inhibiting the co-expression and indirect interaction between peripheral TRPV1 and P2X3.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a modely nemocí na zvířatech $7 D004195
- 650 12
- $a elektroakupunktura $7 D015671
- 650 _2
- $a spinální ganglia $x metabolismus $x patofyziologie $7 D005727
- 650 _2
- $a hyperalgezie $x metabolismus $x patofyziologie $x terapie $7 D006930
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a neuralgie $x metabolismus $x patofyziologie $x terapie $7 D009437
- 650 _2
- $a práh bolesti $7 D017288
- 650 _2
- $a potkani Sprague-Dawley $7 D017207
- 650 _2
- $a purinergní receptory P2X3 $x metabolismus $7 D058477
- 650 _2
- $a signální transdukce $7 D015398
- 650 _2
- $a kationtové kanály TRPV $x metabolismus $7 D050916
- 655 _2
- $a srovnávací studie $7 D003160
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Du, Junying $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 700 1_
- $a Fang, Junfan $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 700 1_
- $a Xiang, Xuaner $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 700 1_
- $a Xu, Yingling $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 700 1_
- $a Wang, Sisi $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 700 1_
- $a Sun, Haiju $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 700 1_
- $a Fang, Jianqiao $u Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, China
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 70, č. 4 (2021), s. 635-647
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/34062076 $y Pubmed
- 910 __
- $a ABA008 $b A 4120 $c 266 $y p $z 0
- 990 __
- $a 20220309 $b ABA008
- 991 __
- $a 20220323102113 $b ABA008
- 999 __
- $a ok $b bmc $g 1773036 $s 1159099
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2021 $b 70 $c 4 $d 635-647 $e 20210601 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- LZP __
- $b NLK118 $a Pubmed-20220309