m-3M3FBS acts as a potent activator of phospholipase C (PLC), enhancing superoxide production in human neutrophils, increasing intracellular calcium levels, and promoting inositol phosphate generation across various cell lines, leading to apoptosis in monocytic leukemia cells[1].[2].[3].
体外研究
m-3M3FBS triggers the production of inositol phosphates in U937 cells within a concentration range of 5-50 μM[1].
At a 50 μM concentration over 24 hours, m-3M3FBS hampers the proliferation of leukemia cell lines U937 and THP-1 without affecting primary monocytes[3].
Furthermore, under the same conditions, it provokes apoptosis in U937 cells[3].
m-3M3FBS 细胞实验
Cell Line
Concentration
Treated Time
Description
References
mouse peritoneal macrophages
10 mM
30 minutes
inhibited TAK1 phosphorylation and activation of the MAPKs and NF-κB pathways
Nat Commun. 2019 Feb 14;10(1):746
HCT 116 cells
25 μM
Induced intracellular Ca2+ release, leading to mitochondrial inner membrane permeabilization (MIMP) and cell death
Cell Death Differ. 2022 Jul;29(7):1318-1334
HeLa cells
25 μM
approx. 200–400 s
Induced intracellular Ca2+ release, leading to mitochondrial inner membrane permeabilization (MIMP) and cell death
Cell Death Differ. 2022 Jul;29(7):1318-1334
rat hippocampal CA1 pyramidal cells
30 μM
60 seconds
restore PLCβ-dependent S-eCB mobilization disrupted by AβO
Alzheimers Res Ther. 2021 Oct 8;13(1):165
CHO cells (Chinese hamster ovary cells)
25 μM
m-3M3FBS caused a slowly developing Ca2+ elevation, though of lower magnitude than in SH-SY5Y cells. No inositol phosphate elevation was observed after 20 minutes of stimulation.
Br J Pharmacol. 2004 Sep;143(1):3-7
SH-SY5Y human neuroblastoma cells
25 μM
4-6 minutes
m-3M3FBS caused a slowly developing Ca2+ elevation, indicating Ca2+ release from intracellular stores such as endoplasmic reticulum and mitochondria. No PLC activation was detected within the time frame of Ca2+ elevation (up to 7 minutes).
Br J Pharmacol. 2004 Sep;143(1):3-7
mouse ventricular myocytes
25 μM
m-3M3FBS (a putative PLC activator) suppressed the activation of VRAC current, and this effect was reversed by intracellular excess PIP2
Br J Pharmacol. 2010 Sep;161(1):193-206
Aplysia bag cell neurons
25 μM
20 min
Activation of PLC, mimicking DAG release, induces inward current
J Physiol. 2016 Oct 1;594(19):5573-92
WEHI-231 cells
50 μM
Activated PLC, thereby activating LK bg channels
J Physiol. 2007 Aug 1;582(Pt 3):977-90
platelets
100, 200, 400 μM
m-3M3FBS, as a direct PLC activator, dose-dependently activated platelet PLCγ2 and induced platelet aggregation. Fc pretreatment partially restored m-3M3FBS-induced platelet aggregation.
Front Pharmacol. 2018 Nov 6;9:1293
T-REx-TRPM3 cells
5 μM
3 hours preincubation, 24 hours stimulation
Test the effect of m-3M3FBS on TRPM3 signaling, results showed nearly 98% inhibition of TRPM3 signaling
Int J Mol Sci. 2022 Aug 24;23(17):9590
HEK293-M8 cells
5 μM
3 hours preincubation, 24 hours stimulation
Test the effect of m-3M3FBS on TRPM8 signaling, results showed nearly 90% inhibition of TRPM8 signaling
Int J Mol Sci. 2022 Aug 24;23(17):9590
HEK293 cells
1 μM
24 hours
Test the effect of m-3M3FBS on AP-1 activity, results showed 1 μM concentration marginally activated AP-1 activity
Int J Mol Sci. 2022 Aug 24;23(17):9590
m-3M3FBS 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
Plcb2 knockout mice
Intraperitoneal injection
5 mg/kg
Three times (1 day before, 2 days after, and 5 days after infection)
Alleviated CVA16 infection-induced histopathology and prolonged survival
Nat Commun. 2019 Feb 14;10(1):746
5XFAD mice
Alzheimer's disease model
Direct hippocampal injection
50 μM
Single injection, 3-day recovery
Restore hippocampus-dependent contextual fear memory
Alzheimers Res Ther. 2021 Oct 8;13(1):165
Least shrew (Cryptotis parva)
Model of vomiting
Intraperitoneal (i.p.)
50 mg/kg
Single dose, observed for 2 hours
To investigate the emetic potential of m-3M3FBS in the least shrew model of vomiting. It was found that a 50 mg/kg dose induced vomiting in ～90% of tested shrews, accompanied by significant increases in c-Fos expression and ERK1/2 phosphorylation in the brainstem dorsal vagal complex.
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