Pectolinarigenin, as a flavonoids compound, which can be isolated from the aerial parts of C. chanroenicum has been displayed biologic activities such as anti-inflammation and anti-allergy[1]. It also repressed cancer growth in vitro, including lung cancer, breast cancer and colorectal adenocarcinoma[2].
In vitro, pectolinarigenin inhibited significantly the growth of the SK-HEP-1 liver cancer cells and exhibited an IC50 of 10 µM, while against normal cells the cytotoxic effects were much less pronounced[3]. In vitro experiment it demenstrated that Pectolinarigenin at 10 µM obviously inhibited ROS accumulation after 24 h-treatment in HepG2 cells and also increased protein expression of NQO-1 and AKR1B10[4]. In vitro, 30 µM pectolinarigenin treatment suppressed melanin biosynthesis without cytotoxicity in melan-a cells[5]. Pectolinarigenin also reduced the lipid contents in vitro[6]. Treatment with 40 µM pectolinarigenin in A375 cells and in B16 cells increased >6-fold and 10-fold apoptotic rate compared with the respective untreated control groups[7].
In vivo, 10 mg/kg pectolinarigenin in mice could activate the Nrf2/ARE pathway and induced antioxidant enzymes as the same manner as the results from HepG2 cells[4]. In vivo efficacy test it shown that mice were administrated pectolinarigenin (20 mg/kg/2 days and 50 mg/kg/2 days) intraperitoneally blocked STAT3 activation and disturbed tumor growth and metastasis with superior pharmacodynamic properties[8]. In vivo test it exhibited that mice were administrated with 25 mg/kg/d orally for 7 days or 14 days effectively ameliorated kidney injury and tubulointerstitial fibrosis after unilateral ureteral obstruction (UUO) surgery[9].
References:
[1] H. Lim, et al. Anti-inflammatory activity of pectolinarigenin and pectolinarin isolated from Cirsium chanroenicum Biol. Pharm. Bull., 31 (2008), pp. 2063-2067.
[2] M. Bonesi, et al. In vitro biological evaluation of novel 7-O dialkylaminoalkyl cytotoxic pectolinarigenin derivatives against a panel of human cancer cell lines Bioorg. Med. Chem. Lett., 18 (2008), pp. 5431-5434.
[3] Liu S, et al. Pectolinarigenin flavonoid exhibits selective anti-proliferative activity in cisplatin-resistant hepatocellular carcinoma, autophagy activation, inhibiting cell migration and invasion, G2/M phase cell cycle arrest and targeting ERK1/2 MAP kinases. J BUON. 2020 Jan-Feb;25(1):415-420.
[4] Shiraiwa M, et al. Pectolinarigenin Induces Antioxidant Enzymes through Nrf2/ARE Pathway in HepG2 Cells. Antioxidants (Basel). 2022 Mar 30;11(4):675.
[5] Lee S, et al. Pectolinarigenin, an aglycone of pectolinarin, has more potent inhibitory activities on melanogenesis than pectolinarin. Biochem Biophys Res Commun. 2017;493:765-772.
[6] Zhang Y, Wan C, Song Z, Meng W, Wang S, Lan Z. Pectolinarigenin reduces the expression of sterol regulatory element-binding proteins and cellular lipid levels. Biosci Biotechnol Biochem. 2022 Aug 24;86(9):1220-1230.
[7] Deng Y, et al. Pectolinarigenin inhibits cell viability, migration and invasion and induces apoptosis via a ROS-mitochondrial apoptotic pathway in melanoma cells. Oncol Lett. 2020 Oct;20(4):116.
[8] Zhang T, et al. Pectolinarigenin acts as a potential anti-osteosarcoma agent via mediating SHP-1/JAK2/STAT3 signaling. Biomed Pharmacother. 2022 Sep;153:113323.
[9] Li Y, et al. Natural flavonoid pectolinarigenin alleviated kidney fibrosis via inhibiting the activation of TGFβ/SMAD3 and JAK2/STAT3 signaling. Int Immunopharmacol. 2021 Feb;91:107279.
柳穿鱼黄素作为一种黄酮类化合物,从紫薇地上部分分离得到且已显示出抗炎、抗过敏等生物活性[1]。它还抑制了体外癌症的生长,包括癌症、乳腺癌和大肠腺癌[2]。
在体外,柳穿鱼黄素抑制剂显著抑制SK-HEP-1肝癌细胞的生长,IC50为10 µM,而对正常细胞的细胞毒作用则不太明显[3]。体外实验表明,10 µM的柳穿鱼黄素在HepG2细胞中处理24小时后明显抑制了ROS的积累,并增加了NQO-1和AKR1B10的蛋白质表达[4]。在体外,30 µM柳穿鱼黄素处理抑制黑色素生物合成,而不会对黑色素a细胞产生细胞毒性[5]。柳穿鱼黄素在体外也能降低脂质含量[6]。与未经处理的对照组相比,在A375细胞和B16细胞中用40 µM柳穿鱼黄素处理的凋亡率增加了>6倍和10倍[7]。
在体内,小鼠中10 mg/kg的柳穿鱼黄素可以激活Nrf2/ARE途径并诱导抗氧化酶,其方式与HepG2细胞的结果相同[4]。体内药效试验表明,小鼠腹腔给药柳穿鱼黄素(20 mg/kg/2天和50 mg/kg/2天)阻断STAT3激活并干扰肿瘤生长和转移,具有优越的药效学特性[8]。体内试验表明,小鼠口服25 mg/kg/d柳穿鱼黄素,持续7天或14天,可有效改善单侧输尿管梗阻(UUO)手术后的肾损伤和肾小管间质纤维化[9]。