**Background**
Inflammation and vascular dysfunction are central to the pathogenesis of numerous diseases, ranging from allergic dermatitis and ischemic stroke to autoimmune hepatitis and diabetic peripheral neuropathy. The ability to protect the blood-brain barrier (BBB) and modulate immune responses is critical for developing therapies that reduce tissue damage and edema. Furthermore, the development of selective agents that can induce apoptosis in malignant cells while maintaining vasoprotective properties is a significant area of biomedical research. In this context, we will introduce a natural triterpenoid saponin compound – Escin.
**Definition**
Escin is a natural compound of triterpenoid saponins isolated from horse chestnut (Aesculus hippocastanum) seeds, utilized as a vasoprotective, anti-inflammatory, anti-edematous, and anti-nociceptive agent.
**In Vitro and In Vivo Studies**
According to the Escin description, this compound exhibits diverse biological activities across various cell lines and animal models. Regarding Escin in vitro activity, Escin (1 μM, 0-5 h) stimulates the phosphorylation of the GR in CFTL-12 murine mast cells. In bEnd.3 cells, Escin (0.1-1 µg/mL, 24 h) protects against OGD/R and rt-PA stimulated damage, upregulating the expression of ZO-1 and Occludin. In the context of Escin Cancer research, Escin (0-100 μg/mL, 12-48 h) induces cell cycle arrest and apoptosis in HCT116 and HCT8 colorectal cancer cells, while Escin (0-80 μg/mL, 12-24 h) upregulates p-ATM and γH2AX, inducing DNA damage. Additionally, Escin (0-50 μM, 24 h) induces apoptosis in T24 and J82 bladder cancer cells by generating ROS and decreasing mitochondrial membrane potential.
Escin in vivo studies further demonstrate its therapeutic potential. Escin (1-5 mg/kg, p.o.) inhibits allergic skin responses in porcine models. In mice, Escin (0.5 and 1 mg/kg, i.v.) attenuates rt-PA induced hemorrhagic transformation. Furthermore, Escin (10 mg/kg, p.o., 4 days) provides antioxidant and anti-inflammatory effects against Con A-induced immune-mediated hepatitis, decreasing peak activities of ALT, AST, and LDH. Finally, Escin (5-20 mg/kg, p.o.) alleviates peripheral neuropathy in streptozotocin-induced diabetic rats. In conclusion, Escin is a versatile triterpenoid saponin with potent vasoprotective and antitumor properties.
Keywords
Escin, 6805-41-0, Apoptosis, anti-inflammatory, anti-edematous, anti-nociceptive, tumor, Inhibitor, inhibitor, inhibit
References
[1] Sipos W, et al. Escin inhibits type I allergic dermatitis in a novel porcine model. Int Arch Allergy Immunol. 2013;161(1):44-52.
[2] Sun X, et al. Escin avoids hemorrhagic transformation in ischemic stroke by protecting BBB through the AMPK/Cav-1/MMP-9 pathway. Phytomedicine. 2023 Nov;120:155071.
[3] Elshal M, Hazem SH. Escin suppresses immune cell infiltration and selectively modulates Nrf2/HO-1, TNF-α/JNK, and IL-22/STAT3 signaling pathways in concanavalin A-induced autoimmune hepatitis in mice. Inflammopharmacology. 2022 Dec;30(6):2317-2329.
[4] Suryavanshi SV, Kulkarni YA. Escin alleviates peripheral neuropathy in streptozotocin induced diabetes in rats. Life Sci. 2020 Aug 1;254:117777.
[5] Wang Z, et al. Escin-induced DNA damage promotes escin-induced apoptosis in human colorectal cancer cells via p62 regulation of the ATM/γH2AX pathway. Acta Pharmacol Sin. 2018 Oct;39(10):1645-1660.
[6] Cheng CL, et al. Escin induces apoptosis in human bladder cancer cells: An in vitro and in vivo study. Eur J Pharmacol. 2018 Dec 5;840:79-88.