Larixyl acetate (5 mg/kg, i.p., once dailly for 7 days) significantly improves aortic endothelial dysfunction in TBI mice by inhibiting TRPC6 activity, particularly enhancing acetylcholine-induced dilation[3].
Larixyl acetate (5 mg/kg, i.p., once daily for 4 weeks) improves cardiac function in pressure overload-induced heart failure model by inhibiting TRPC6, reducing cardiac hypertrophy, fibrosis, and apoptosis[4].
| Animal Model: | Closed-head mild traumatic brain injury (mTBI) model, C57BL/6, 129S, 129S-C57BL/6-F2 mice, TRPC6 knockout mice[3] |
| Dosage: | 5 mg/kg |
| Administration: | Intraperitoneal injection (i.p.), once daily for 7 days |
| Result: | Significantly improved aortic endothelial function 7 days after TBI.
Caused that acetylcholine (10 μM) induced dilation was significantly enhanced in Larixyl acetate-treated mice (In C57BL/6 mice, the Larixyl acetate group showed 96.9 %; in 129S-C57BL/6-F2 mice, the Larixyl acetate group showed 89.2 %). |
| Animal Model: | Transverse aortic constriction (Tac) model for pressure overload-induced heart failure in mice[5] |
| Dosage: | 5 mg/kg |
| Administration: | Intraperitoneal injection (i.p.), once daily for 4 weeks |
| Result: | Significantly reduced cardiac hypertrophy, left ventricular pressure, and improved cardiac function (FS and EF increased).
Improved TAC-induced cardiac fibrosis, cardiomyocyte apoptosis, and inhibited ER stress-related proteins (e.g., GRP78) expression. |
