Animal experiment:

Rats[1]A total of 50 adult male Sprague Dawley rats (age, 7 8 weeks; weight, 260 280 g) are used. Rats are randomly assigned into five groups (n=10 in each). Rats in the control group undergo sham surgery. All other rats undergo suture occluded surgery, with a 0.26 mm nylon monofilament inserted through the right common carotid artery and are divided into groups as follows: The cerebral I/R injury model group (model), no treatment; low dose group, 30 mg/kg/day Morroniside by gavage; moderate dose group, 90 mg/kg/day Morroniside by gavage; high dose group, 270 mg/kg/day Morroniside by gavage. Rats in the control and model groups receive an equal volume of normal saline[1].

Morroniside has neuroprotective effect by inhibiting neuron apoptosis and MMP2/9 expression.

Morroniside reduces the expression of MMP2 and MMP9 in an I/R injury model. Treatment with Morroniside significantly reduces I/R-associated neuron apoptosis in a dose dependent manner. The results demonstrate that active caspase-3 and Bax are significantly upregulated in the model group compared with the control group, while Bcl-2 is significantly downregulated. The expression of active caspase-3 and Bax is significantly downregulated by Morroniside treatment in a dose-dependent manner, while the expression of Bcl-2 is significantly upregulated[1]. Morroniside has an ameliorative effect on diabetes-induced alterations such as oxidative stress, inflammation, and apoptosis in the liver of type 2 diabetic db/db mice[2].

References:
[1]. Zeng G, et al. Morroniside protects against cerebral ischemia/reperfusion injury by inhibiting neuron apoptosis and MMP2/9 expression. Exp Ther Med. 2018 Sep;16(3):2229-2234.
[2]. Park CH, et al. Evaluation of morroniside, iridoid glycoside from Corni Fructus, on diabetes-induced alterations such as oxidative stress, inflammation, and apoptosis in the liver of type 2 diabetic db/db mice. Biol Pharm Bull. 2011;34(10):1559-65.