TJ-17 (Goreisan) mitigates renal fibrosis in a mouse model of folic acid-induced chronic kidney disease

Suenaga, A.; Seto, Yasuyuki; Funamoto, Masafumi; Imanishi, Masaki; Tsuchiya, Koichiro; Ikeda, Yasumasa

doi:10.1016/j.jphs.2023.07.001

Cited by 1 publication

(2 citation statements)

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“…The diuretic effect of GRS demonstrated in this study is attributable to the CaSR-mediated regulation of AQP2 translocation in response to various stimuli. Conversely, GRS has been demonstrated to exert antiin ammatory and anti-brotic effects on renal injury with renal substrate changes attributable to 5/6 nephrectomy and drug-induced in ammation and brosis and to improve urine concentrating ability by correcting the changes in AQP2 gene expression [6,7] . It has been reported that CaSR is involved in both the localization of AQP2 and the regulation of gene and protein expression via microRNA and/or the ubiquitin-proteasome axis [33] .…”

Section: Discussionmentioning

confidence: 99%

“…Several studies revealed that AQPs are involved in the effects of GRS. It is known that GRS can regulate urinary volume by modulating the gene expression of AQP1, AQP2, and AQP3 in partial nephrectomy and drug-induced kidney disease models [6,7] . In the lipopolysaccharide-induced diarrhea model, GRS ameliorated the in ammation-associated downregulation of AQP3 in the intestinal tract and improved diarrhea symptoms [8] .…”

Section: Introductionmentioning

confidence: 99%

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The diuretic effect of Goreisan involves the modulation of aquaporin 2 localization via the calcium-sensing receptor

Ogura,

Fujitsuka,

Nahata

et al. 2024

Preprint

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Aquaporin 2 (AQP2) contributes to water reabsorption and primitive urine concentration by migrating to the luminal surface of the collecting ducts in an anti-diuretic hormone-stimulated manner, and the signaling pathway involved in AQP2 localization is a target for diuretics. This study investigated whether AQP2 is involved in the diuretic effect and mechanisms of Goreisan (GRS), a traditional Japanese Kampo medicine used to treat symptoms such as edema in patients with decreased urination. GRS exerted diuretic effects on desmopressin (dDAVP)-induced decreases in urine output and inhibited phosphorylation of AQP2 at Ser269 in the renal tissues of mice. Furthermore, GRS inhibited the migration of phosphorylated AQP2 to the luminal side following forskolin (FSK) stimulation using a 3D culture model of the kidney collecting duct cell line mIMCD-3. GRS induced a transient increase in the intracellular calcium concentration via the calcium-sensing receptor (CaSR) and suppressed the FSK-stimulated increase in cAMP production. These results suggest that GRS regulates urine volume by modulating the localization of AQP2 via CaSR.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%