Diosmin is a flavonoid found in a variety of citrus fruits and also an agonist of the aryl hydrocarbon receptor (AhR). Diosmin is known to exhibit anti-inflammatory, antimutagenic, antioxidant, and free radical scavenging as well as blood lipid lowering activities among others. Diosmin-100 and Diosmin-200 significantly attenuated the damage to lung epithelium, alveolar architecture, and reduced inflammatory cell infiltration in the lung tissues of mice. Diosmin significantly attenuated the levels of oxidative stress markers: lactate dehydrogenase and xanthine oxidase[3]. At 5 μM, Diosmin increases the cytotoxicity of 7,12-dimethylbenz(a)anthracene (DMBA), shifting the IC50 of DMBA from an estimated 1.2 μM to 400 nM. Diosmin is not cytotoxic in itself at the concentrations tested. Diosmin causes an increase in CYPIAI activity in MCF-7 cells in a time- and dose-dependent fashion[4]. Diosmin protected the retina from I/R injury, possibly via a mechanism involving the regulation of oxidative parameters[5]. Moreover, diosmin is able to induce caspase-dependent apoptosis specifically in tumor cells and, therefore, could be considered a promising therapeutic compound against glioblastoma[6].
77-67-8 Ethosuximide
Ethosuximide, 2-ethyl-2-methylsuccinimide, has been used extensively for "petit mal" seizures. Commonly observed side effects of ethosuximide are dose dependent and involve the gastrointestinal tract and central nervous system. The spontaneous pacemaker oscillatory activity of thalamocortical circuitry involves low threshold T-type Ca2+ currents in the thalamus, and ethosuximide is presumed to reduce these low threshold T-type Ca2+ currents in thalamic neurons. Ethosuximide also decreases the persistent Na+ and Ca2+ -activated K+ currents in thalamic and layer V cortical pyramidal neurons[7]. Ethosuximide and valproic acid are more effective than lamotrigine in the treatment of childhood absence epilepsy. Ethosuximide is associated with fewer adverse attentional effects[8]. Concentrations of 2 μM or more of Ethosuximide not only are found to be less effective than 1 μM concentration of Ethosuximide, but also induce cell toxicity. The number and percentage of tubulin β-III immunopositive neurons were increased after 6 days treatment with ethosuximide. Ethosuximide may compensate damage caused by seizure attacks and possibly other neuronal loss disorders[9]. Ethosuximide given with drinking water (300 mg/kg/day) over 45 days slightly reduced proneness to audiogenic epilepsy and increased locomotor activity of the animals at the periphery of the open field. A weak anticonvulsant effect of ethosuximide on tonic convulsions with its predominant effect on convulsions with forebrain focus location[10].
Diosmin/地奥司明 细胞实验
Cell Line
Concentration
Treated Time
Description
References
C2C12 mouse myoblasts
0, 5, 10, 50, 100 μM
24 h
To investigate the effect of diosmin on the proliferation of C2C12 myoblasts. Results showed that 10, 50, and 100 μM diosmin significantly promoted the viability of C2C12 myoblasts, and 50 μM diosmin markedly increased the protein expression of proliferating cell nuclear antigen (Pcna), accelerated the G1/S phase transition, thereby enhancing the proliferation ability of C2C12 myoblasts.
J Agric Food Chem. 2023 Dec 13;71(49):19705-19716.
N2a cells
80 µM
12 h
Diosmin significantly increased NEP expression and enzyme activity
Theranostics. 2021 Aug 11;11(18):8797-8812.
CHO-K1 cells
0.01–1 μM
24 h
Diosmin effectively activated the I-R gene via inducing opioid secretion, showing utility as an antidiabetic drug.
Nutrients. 2020 Sep 23;12(10):2907.
Diosmin/地奥司明 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
ICR mice
Muscle injury model
Intraperitoneal injection
0, 10, 30 mg/kg
Two consecutive days, once daily
To explore the effect of diosmin on muscle injury repair. Results showed that diosmin promoted myoblast proliferation by activating the Akt/FOXO1 pathway, increased the number of central nuclei of newly formed muscle fibers and the proportion of muscle fibers with large cross-sectional area (CSA), and had a positive effect on muscle repair injury.
J Agric Food Chem. 2023 Dec 13;71(49):19705-19716.
APP/PS1 transgenic mice
Alzheimer's disease model
Oral
40 mg/kg
Once daily for 4 weeks
Diosmin ameliorated cognitive deficits by activating AhR and increasing NEP expression
Theranostics. 2021 Aug 11;11(18):8797-8812.
Wistar rats
Complete Freund’s adjuvant-induced arthritis model
Oral
20 mg/kg
Once daily for 2 weeks
To evaluate the anti-arthritic, anti-inflammatory, and antioxidant effects of diosmin and/or trolox in CFA-induced arthritic rats. Results showed that diosmin and/or trolox significantly reduced serum levels of RF, ACPA, TNF-α, and IL-17, increased IL-13 levels, improved markers of oxidative stress and the antioxidant defense system, and exerted anti-arthritic effects by suppressing NF-κB signaling, activating Nrf2, and inhibiting matrix metalloproteinases (MMPs).
Antioxidants (Basel). 2022 Aug 30;11(9):1721
Male Wistar rats
Doxorubicin-induced liver injury model
Oral gavage
100 and 200 mg/kg
Administered daily for the first 18 days and then exposed to DOX on day 17
Diosmin pretreatment significantly restored the DOX-induced increase in serum ALT, AST, and ALP levels, reduced the oxidative stress marker MDA, and restored GSH levels and CAT activity. Additionally, diosmin mitigated inflammation and apoptosis-related protein expression by modulating the NF-κB and MAPK pathways.
Antioxidants (Basel). 2021 Dec 15;10(12):1998
Sprague-Dawley rats
L-NAME-induced hypertensive model
Mixed with powdered food
7.16 mg/kg
Daily administration for 6 weeks
To evaluate the antihypertensive effect of Diosmin and its impact on vascular and renal function in L-NAME-induced hypertensive rats. Results showed that Diosmin partially improved vasodilation, reduced oxidative stress markers, and decreased aortic wall thickness.
搜索
