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These results suggest that ginsenoside-Rd, as an inhibitor, remarkably inhibits Ca2+ entry through ROCC and SOCC without effects on VDCC and Ca2+ release in vascular smooth muscle cells.
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Pharmacological inhibition of xCT remarkably inhibited proliferation of multiple cancer cells in vitro and attenuated tumour growth in vivo [ 13, 17].
The POD activity was remarkably inhibited by large quantity of ZnO nanoparticles (50 mg/L).
The CE-ECM scaffold facilitated chondrogenesis, however the CL-ECM scaffolds remarkably inhibited chondrogenesis of MSCs.
Additionally, GSK3β siRNA remarkably inhibited Wnt5a-induced RhoA activation, stress fiber formation and cell migration.
Overexpression of let-7c-5p in BV2 cells remarkably inhibited the microglial activation.
More significantly, this active scaffold remarkably inhibited the interaction between IN and LEDGF/p75 cofactor.
VKJP1 and VKJP3 also remarkably inhibited the transport of [3H]-methotrexate [3H]-methotrexate vesicles.
In mesangial cells, PMQ remarkably inhibited the cell proliferation and total collagen accumulation, and suppressed cell hypertrophy.
OA remarkably inhibited the intestinal PP activity but it recovered to the normal levels within 6 to 24 h.
Additionally, compound 25h could remarkably inhibit cancer growth in established HCC827 xenograft mouse model at 50 mg/kg in vivo.
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