ArticleWorld journal of gastroenterology2005
Tetramethylpyrazine stimulates cystic fibrosis transmembrane conductance regulator-mediated anion secretion in distal colon of rodents.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- CFTR chloride channel as a molecular target of anthraquinone compounds in herbal laxatives.Acta pharmacologica Sinica · 2011Article
- Stimulation of Airway and Intestinal Mucosal Secretion by Natural Coumarin CFTR Activators.Frontiers in pharmacology · 2011Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the effect of tetramethylpyrazine (TMP), an active compound from Ligustium Wollichii Franchat, on electrolyte transport across the distal colon of rodents and the mechanism involved.
methodsThe short-circuit current (I(SC)) technique in conjunction with pharmacological agents and specific inhibitors were used in analyzing the electrolyte transport across the distal colon of rodents. The underlying cellular signaling mechanism was investigated by radioimmunoassay analysis (RIA) and a special mouse model of cystic fibrosis.
resultsTMP stimulated a concentration-dependent rise in I(SC), which was dependent on both Cl(-) and HCO(3)(-), and inhibited by apical application of diphenylamine-2,2'-dicarboxylic acid (DPC) and glibenclamide, but resistant to 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate (DIDS). Removal of Na(+) from basolateral solution almost completely abolished the I(SC) response to TMP, but it was insensitive to apical Na(+) replacement or apical Na(+) channel blocker, amiloride. Pretreatment of colonic mucosa with BAPTA-AM, a membrane-permeable selective Ca(2+) chelator, did not significantly alter the TMP-induced I(SC). No additive effect of forskolin and 3-isobutyl-1-methylxanthine (IBMX) was observed on the TMP-induced I(SC), but it was significantly reduced by a protein kinase A inhibitor, H(89). RIA results showed that TMP (1 mmol/L) elicited a significant increase in cellular cAMP production, which was similar to that elicited by the adenylate cyclase activator, forskolin (10 micromol/L). The TMP-elicited I(SC) as well as forskolin- or IBMX-induced I(SC) were abolished in mice with homozygous mutation of the cystic fibrosis transmembrane conductance regulator (CFTR) presenting defective CFTR functions and secretions.
conclusionTMP may stimulate cAMP-dependent and CFTR-mediated Cl(-) and HCO(3)(-) secretion. This may have implications in the future development of alternative treatment for constipation.
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