To evaluate the protective effects of Tilianin against OGD/R-induced injury in H9c2 cells. Results showed Tilianin significantly enhanced cell viability, inhibited TLR4/NF-κB pathway and NLRP3 inflammasome activation, and reduced ASC speck formation and inflammatory cytokine release.
Front Pharmacol. 2024 Oct 23;15:1423053
SH-SY5Y cells
10 mM and 30 mM
24 hours
Tilianin increased the downregulated miR-193b-3p and miR-152-3p levels in OGD-injured SH-SY5Y cells.
Front Immunol. 2023 Apr 19;14:1118808
FaDu cells
10, 30, 100 µM
24 hours (apoptosis assay), 48 hours (qPCR, Western blot, ELISA analyses), 14 days (plate clone formation assay)
Tilianin inhibited FaDu cell proliferation and induced apoptosis in a dose-dependent manner. It upregulated pro-apoptotic factors Bax and Bad, downregulated anti-apoptotic factors Bcl-2 and Bcl-xL, activated caspase-3 and PARP, and stimulated cytochrome c release, thereby inducing apoptosis via the mitochondrion-dependent intrinsic apoptotic pathway.
Front Pharmacol. 2020 Mar 4;11:205
Tilianin/田蓟苷 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Sprague-Dawley rats
Myocardial ischemia/reperfusion injury model (LAD ligation/release)
Intraperitoneal injection
3, 10, 30 mg/kg
Single dose at reperfusion onset, lasting 24 h
To investigate the cardioprotective mechanisms of Tilianin in MIRI. Results demonstrated Tilianin improved cardiac function (reduced LVESD, increased LVEF/LVFS), decreased infarct size and apoptosis, and suppressed TLR4/NF-κB/NLRP3 pathway and inflammatory cytokines (IL-1β, IL-18) release.
Front Pharmacol. 2024 Oct 23;15:1423053
Sprague-Dawley rats
2VO vascular dementia model
Oral
40 mg/kg
Once daily for four weeks
Tilianin ameliorated cognitive deficits, neurodegeneration, and microglial and astrocytic activation in rats with 2VO.
Front Immunol. 2023 Apr 19;14:1118808
C57BL/6 mice
Ischemia/reperfusion-induced acute kidney injury model
Intragastric administration
5 mg/kg, 10 mg/kg, 15 mg/kg
Once daily for 7 days
Tilianin reduces apoptosis via the ERK/EGR1/BCL2L1 pathway in ischemia/reperfusion-induced acute kidney injury mice.
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