Ophiopogonoside B

Ophiopogonoside B is a naturally occurring eudesmane-type sesquiterpene glycoside isolated from the tuberous roots of Liriope muscari. Bioactivity studies have shown that Ophiopogonoside B exhibits moderate inhibitory activity against glycogen phosphorylase a. In addition, Ophiopogonoside B also holds potential application value in anti-lung cancer metastasis and anti-angiogenesis.

GPa:88.30 μM

Method: Glycogen phosphorylase a (Gpa) extracted from rabbit liver was used, and ophiopogonoside B was added to the enzyme reaction system. Phosphate absorbance was monitored at 620 nm using a microplate reader, and the inhibition rate and IC50 value were calculated.
Result: Ophiopogonoside B exhibited moderate inhibitory activity against glycogen phosphorylase a, with an IC50 value of 88.30 μM [1].
Method: Human hepatocellular carcinoma MHCC97-H cells were treated with ophiopogonoside B (5, 10, 20, 40 μM) for 24 h, and cell viability was assessed using the CCK-8 assay.
Result: Ophiopogonoside B inhibited MHCC97-H cell viability in a concentration-dependent manner, reducing viability to below 50% at 40 μM, while showing no significant effect on normal hepatocyte HHL-5 cells [2].
Method: MHCC97-H cells were treated with ophiopogonoside B (20 μM), and colony formation, TUNEL staining, and Western blot were used to detect cell proliferation, apoptosis, and related protein expression.
Result: Ophiopogonoside B significantly suppressed colony formation, induced apoptosis, upregulated the expression of Bax, cleaved caspase-3, and cleaved PARP, and downregulated Bcl-2 expression [2].
Method: Human lung adenocarcinoma A549 cells were treated with ophiopogonoside B (2.5, 5, 10 μM) for 24 h, and cell migration and invasion abilities were assessed using Transwell and wound healing assays.
Result: Ophiopogonoside B (10 μM) significantly inhibited the migration and invasion of A549 cells [3].
Method: A549 cells were treated with ophiopogonoside B (10 μM) for 24 h, and Western blot was used to detect the expression of EMT-related proteins and proteins in the Src/FAK/Stat pathway.
Result: Ophiopogonoside B upregulated the epithelial markers E-cadherin and ZO-1, downregulated the mesenchymal marker N-cadherin and the transcriptional repressors Snail, Slug, and ZEB1, while also inhibiting the phosphorylation of Src, FAK, Stat3, and Stat5 [3].

Method: Male BALB/c nude mice were subcutaneously inoculated with MHCC97-H cells to establish an HCC xenograft model. The mice were divided into a control group, an Ophiopogonoside B 15 mg/kg group, and a 75 mg/kg group (n = 5 per group). Drugs were administered daily by gavage for 21 consecutive days. Tumor volume and weight were measured, and immunohistochemistry (IHC) was used to detect the expression of Ki67, CD31, and VEGFA.
Result: Ophiopogonoside B at both 15 and 75 mg/kg significantly inhibited tumor growth, reduced tumor weight and the tumor/body weight ratio, and decreased the expression of Ki67, CD31, and VEGFA. Moreover, it downregulated the mRNA and protein levels of PTP1B in tumor tissues. However, a significant decrease in body weight was observed in the 75 mg/kg group on day 21 [2].
Method: Nude mice were subcutaneously injected with a mixture of A549 cells and Matrigel to establish a xenograft tumor model. The mice were divided into a control group, an Ophiopogonoside B 37.5 mg/kg group, and a 75 mg/kg group (n = 6 per group). Drugs were administered daily by gavage for 14 consecutive days, after which the Matrigel plugs were isolated and hemoglobin content was measured.
Result: Ophiopogonoside B (at 37.5 and 75 mg/kg) significantly inhibited tumor angiogenesis, as evidenced by reduced hemoglobin content in the Matrigel plugs [3].