College of Pharmacy and Medical Research Center, Chungbuk National University, Gaeshin-dong, Heungduk-gu, Cheongju, Chungbuk, Korea.
Prostate. 2011 Jun 1;71(8):801-12. doi: 10.1002/pros.21296. Epub 2010 Nov 17.
Bee venom has been used as a traditional medicine to treat arthritis, rheumatism, back pain, cancerous tumors, and skin diseases. However, the effects of bee venom on the prostate cancer and their action mechanisms have not been reported yet.
To determine the effect of bee venom and its major component, melittin on the prostate cancer cells, apoptosis is analyzed by tunnel assay and apoptotic gene expression. For xenograft studies, bee venom was administrated intraperitoneally twice per week for 4 weeks, and the tumor growth was measured and the tumor were analyzed by immunohistochemistry. To investigate whether bee venom and melittin can inactivate nuclear factor kappa B (NF-κB), we assessed NF-κB activity in vitro and in vivo.
Bee venom (1-10 µg/ml) and melittin (0.5-2.5 µg/ml) inhibited cancer cell growth through induction of apoptotic cell death in LNCaP, DU145, and PC-3 human prostate cancer cells. These effects were mediated by the suppression of constitutively activated NF-κB. Bee venom and melittin decreased anti-apoptotic proteins but induced pro-apoptotic proteins. However, pan caspase inhibitor abolished bee venom and melittin-induced apoptotic cell death and NF-κB inactivation. Bee venom (3-6 mg/kg) administration to nude mice implanted with PC-3 cells resulted in inhibition of tumor growth and activity of NF-κB accompanied with apoptotic cell death. Therefore, these results indicated that bee venom and melittin could inhibit prostate cancer in in vitro and in vivo, and these effects may be related to NF-κB/caspase signal mediated induction of apoptotic cell death.
蜂毒一直被用作传统药物来治疗关节炎、风湿、背痛、癌性肿瘤和皮肤病。然而，蜂毒对前列腺癌的影响及其作用机制尚未报道。
为了确定蜂毒及其主要成分蜂肽对前列腺癌细胞的影响，通过隧道实验和凋亡基因表达分析来分析细胞凋亡。对于异种移植研究，每周两次通过腹腔内给予蜂毒 4 周，测量肿瘤生长，并通过免疫组织化学分析肿瘤。为了研究蜂毒和蜂肽是否可以使核因子 κB（NF-κB）失活，我们评估了体外和体内的 NF-κB 活性。
蜂毒（1-10μg/ml）和蜂肽（0.5-2.5μg/ml）通过诱导 LNCaP、DU145 和 PC-3 人前列腺癌细胞的凋亡性细胞死亡来抑制癌细胞生长。这些作用是通过抑制组成性激活的 NF-κB 介导的。蜂毒和蜂肽降低了抗凋亡蛋白，但诱导了促凋亡蛋白。然而，泛半胱天冬酶抑制剂消除了蜂毒和蜂肽诱导的凋亡性细胞死亡和 NF-κB 失活。给植入 PC-3 细胞的裸鼠给予蜂毒（3-6mg/kg）导致肿瘤生长抑制和 NF-κB 活性伴随凋亡性细胞死亡。因此，这些结果表明蜂毒和蜂肽可以在体外和体内抑制前列腺癌，这些作用可能与 NF-κB/半胱天冬酶信号介导的诱导凋亡性细胞死亡有关。
