Abstract:
:Chlorogenic acid (CGA) is one of the most abundant polyphenol compounds in the human diet. Recently, it is demonstrated to have potent antinociceptive effect. However, little is understood about the mechanism underlying CGA analgesia. Here, we have found that CGA can exert an inhibitory effect on the functional activity of native acid-sensing ion channels (ASICs) in rat dorsal root ganglion (DRG) neurons. First, CGA decreased the peak amplitude of proton-gated currents mediated by ASICs in a concentration-dependent manner. Second, CGA shifted the proton concentration-response curve downward, with a decrease of 41.76 ± 8.65% in the maximum current response to protons but with no significant change in the pH0.5 value. Third, CGA altered acidosis-evoked membrane excitability of rat DRG neurons and caused a significant decrease in the amplitude of the depolarization and the number of action potentials induced by acid stimuli. Finally, peripheral administered CGA attenuated nociceptive response to intraplantar injection of acetic acid in rats. ASICs are distributed in peripheral sensory neurons and participate in nociception. Our findings CGA inhibition of native ASICs indicated that CGA may exert analgesic action by modulating ASICs in the primary afferent neurons, which revealed a novel cellular and molecular mechanism underlying CGA analgesia.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Qu ZW,Liu TT,Qiu CY,Li JD,Hu WPdoi
10.1016/j.neulet.2014.03.027subject
Has Abstractpub_date
2014-05-01 00:00:00pages
35-9eissn
0304-3940issn
1872-7972pii
S0304-3940(14)00226-2journal_volume
567pub_type
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