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A novel polysaccharide was extracted from Coriandrum sativum L. at a yield of 4.56 ± 0.17% (n = 3). The extraction was optimized using response surface methodology: powder-to-liquid ratio 1:21 g/ml, extraction time 188 min, temperature 81°C, and three replicate extractions. The purified polysaccharide had an average molecular weight of 1.30 × 10 6 Da and was composed of rhamnose, arabinose, galactose, glucose, and galacturonic acid in molar ratios of 1.52: 8.14: 20.85:In vivo tests demonstrated that the polysaccharide suppressed H22 tumor growth in mice and protected the immune organs. Annexin V-FITC/PI, PI, and JC-1 staining showed that the primary mechanism of tumor inhibition was the induction of apoptosis and S-phase arrest with apoptosis achieved via a mitochondrial pathway. Practical applicationsCoriandrum sativum L. is used as a culinary spice but its medicinal value has also been widely recognized. A novel polysaccharide was extracted from this herbaceous plant and its structure and bioactivity were investigated. This high-molecular-weight polysaccharide exhibited antitumor effects against H22 cells in mice and had potential to be developed as an anti-liver cancer medicine and functional food supplement.

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This study explored the preliminary structural characteristics and in vivo anti-tumor activity of an acidic water-soluble polysaccharide (BCP) separated purified from Bupleurum chinense DC root. The preliminary structural characterization of BCP was established using UV, HPGPC, FT-IR, IC, NMR, SEM, and Congo red. The results showed BCP as an acidic polysaccharide with an average molecular weight of 2.01 × 103 kDa. Furthermore, we showed that BCP consists of rhamnose, arabinose, galactose, glucose, and galacturonic acid (with a molar ratio of 0.063:0.788:0.841:1:0.196) in both α- and β-type configurations. Using the H22 tumor-bearing mouse model, we assessed the anti-tumor activity of BCP in vivo. The results revealed the inhibitory effects of BCP on H22 tumor growth and the protective actions against tissue damage of thymus and spleen in mice. In addition, the JC-1 FITC-AnnexinV/PI staining and cell cycle analysis have collectively shown that BCP is sufficient to induce apoptosis and of H22 hepatocarcinoma cells in a dose-dependent manner. The inhibitory effect of BCP on tumor growth was likely attributable to the S phase arrest. Overall, our study presented significant anti-liver cancer profiles of BCP and its promising therapeutic potential as a safe and effective anti-tumor natural agent.