Allicin attenuates calcium oxalate crystal deposition in the rat kidney by regulating gap junction function |
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Authors: | Yongchang Lai Xiongfa Liang Fangling Zhong Weizhou Wu Tao Zeng Jian Huang Xiaolu Duan Shujue Li Guohua Zeng Wenqi Wu |
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Institution: | 1. Department of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China;2. Department of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
Guangdong Key Laboratory of Urology, Guangzhou Urology Research Institute, Guangzhou, China
Yongchang Lai, Xiongfa Liang, Fangling Zhong, and Weizhou Wu contributed equally to this work.;3. Department of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
Guangdong Key Laboratory of Urology, Guangzhou Urology Research Institute, Guangzhou, China |
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Abstract: | Renal calculus is a global common urological disease that is closely related to crystal adhesion and renal tubular epithelial cell impairment. Gap junctions (GJs) and their components (connexins and Cxs) are involved in various pathophysiology processes, but their roles in renal calculi progression are not well defined. Our previous RNA microarray analysis suggests that GJs are one of the key predicted pathways involved in the renal calcium oxalate (CaOx) crystal rat model. In the current study, we found that the Cx43 and Cx32 expression and the GJ function decreased significantly after stimulation with CaOx or sodium oxalate (NaOx) in NRK-52E, MDCK, and HK-2 cells, and Cx43 expression also decreased in renal tissues in renal CaOx crystal model rats. Inhibition of Cx43 in NRK-52E cells by small interference RNA significantly increased the CD44 and androgen receptor expression, and the adhesion between CaOx crystals and cells, which were consistent with the function of GJ inhibitors. On the other hand, after GJ function and Cx43 expression were increased by allicin, diallyl disulfide, or diallyl trisulfide, the impairment of NRK-52E cells by NaOx or other GJ inhibitors and the adhesion between CaOx crystals and renal cells decreased significantly. Furthermore, allicin also increased Cx43 expression and inhibited crystal deposition in rat kidneys. Taken together, our results provide a basis that GJs and Cx43 may participate in renal CaOx stone progression and that allicin, together with its analogues, could be potential drugs for renal calculus precaution. |
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Keywords: | allicin calcium oxalate connexin43 gap junction renal calculus |
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