A chloride channel in mouse pancreatic acinar cells is activated by so-dium taurocholate and dependent on extracellular calcium but not reac-tive oxygen species pathway
10.3969/j.issn.1000-4718.2024.10.004
- VernacularTitle:牛磺胆酸钠依赖于胞外钙离子而非活性氧途径激活小鼠胰腺腺泡细胞氯通道
- Author:
Xiaoya YANG
1
;
Jiawei LIN
;
Dong YE
;
Chan ZHAO
;
Liwei WANG
;
Lixin CHEN
Author Information
1. 广州卫生职业技术学院生理学教研室,广东 广州 510450
- Keywords:
sodium taurocholate;
pancreatic acinar cells;
chloride channel;
calcium;
rreactive oxygen species
- From:
Chinese Journal of Pathophysiology
2024;40(10):1806-1814
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the activation of Cl-channels by sodium taurocholate(NaTC)in mouse pan-creatic acinar cells.METHODS:The single isolated pancreatic acinar cells from FVB/N mice were prepared using colla-genase digestion method.Whole-cell patch clamp technique was performed to record the currents.Intracellular adenosine triphosphate(ATP)dependence of the channels was examined via eliminating ATP from the pipette solution.Anion per-meability of the channels was investigated with ion-exchange method.The pharmacological characteristics of the channels was confirmed by two Cl-channel blockers.The volume sensitivity of the channels was detected using 47%hypertonic bathing solution.Extracellular Ca2+dependence of activating the channels was examined through eliminating Ca2+from the bathing solution.Intracellular reactive oxygen species(ROS)level was detected by an oxidation-sensitive fluorescent probe,2',7'-dichlorofluorescin diacetate.The experiment was repeated 6 times in each group.RESULTS:Extracellular application of 5 mmol/L sodium taurocholate induced a Cl-current,exhibiting the properties of outward-rectification,a se-lectivity sequence of I->Br-≥Cl->gluconate-and intracellularATP dependence(P<0.01).The currents were inhibited by chloride channel blocker 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate(DIDS)and tamoxifen and by 47%hypertonicity stimulation(P<0.01).When ROS production was scavenged by N-acetyl-L-cysteine,the sodi-um taurocholate-induced Cl-currents were unaffected.The effect of sodium taurocholate on ROS production did not alter with the treatment with DIDS.Sodium taurocholate failed to induce Cl-currents when Ca2+was absent in extracellular bath-ing solution(P>0.05).CONCLUSION:Sodium taurocholate activates Cl-channels in mouse pancreatic acinar cells,which is dependent on extracellular Ca2+but not ROS pathway.
