Sakai Hiroyasu, Tabata Shoko, Kimura Minami, Yabe Saori, Isa Yosuke, Kai Yuki, Sato Fumiaki, Yumoto Tetsuro, Miyano Kanako, Narita Minoru, Uezono Yasuhito
Department of Analytical Pathophysiology, Division of Pharmacy Professional Development and Research, Hoshi University.
Division of Cancer Pathophysiology, National Cancer Center Research Institute.
Biol Pharm Bull. 2017;40(12):2134-2139. doi: 10.1248/bpb.b17-00479.
5-Fluorouracil (5-FU) is widely used as an anti cancer drug and is known to cause severe diarrhea. Recently we suggested that levels of chemokine (C-X-C motif) ligand 1 (CXCL1) and neutrophil recruitment in the colonic mucosa were drastically increased by the 5-FU administration in mice. Hange-shashin-to (HST) is prescribed in Japan for treat gastritis, stomatitis, and inflammatory diarrhea. We therefore examined the effects of HST and its active ingredients on 5-FU-induced CXCL1 upregulation in cultured colon tissue, and also examined the effects of HST on 5-FU-induced diarrhea development in the mouse. The distal colon isolated from the mouse was incubated with 5-FU and HST. Mice were given 5-FU (50 mg/kg, intraperitoneally (i.p.)) daily for four days. HST (300 mg/kg, per os (p.o.)) was administered 30 min before mice received 5-FU. mRNA levels of CXCL1 in the colon were examined using quantitative RT-PCR. 5-FU enhanced CXCL1 mRNA in the colon but the effect by 5-FU was markedly suppressed by application of HST and its active ingredients, baicalein and 6-gingerol. Nuclear factor kappa B (NF-κB) was activated by 5-FU treatment in cultured colon tissue, which was also suppressed by HST and the combination of baicalein and 6-gingerol. Furthermore, HST reduced 5-FU-induced diarrhea development. Under such experimental condition, CXCL1 gene, protein levels of neutrophil elastase and myeloperoxidase upregulation induced by 5-FU in the colon was attenuated by HST. These findings suggest that HST, especially baicalein and 6-gingerol, prevent the development of neutrophil recruitment and diarrhea by the inhibition of NF-κB activity.
5-氟尿嘧啶(5-FU)作为一种抗癌药物被广泛使用,且已知会导致严重腹泻。最近我们发现,在小鼠中,5-FU给药会使结肠黏膜中趋化因子(C-X-C基序)配体1(CXCL1)水平和中性粒细胞募集显著增加。汉方柴胡汤(HST)在日本被用于治疗胃炎、口腔炎和炎性腹泻。因此,我们研究了HST及其活性成分对培养的结肠组织中5-FU诱导的CXCL1上调的影响,并研究了HST对小鼠中5-FU诱导的腹泻发展的影响。从小鼠分离出的远端结肠与5-FU和HST一起孵育。小鼠连续四天每天腹腔注射(i.p.)5-FU(50 mg/kg)。在小鼠接受5-FU前30分钟口服(p.o.)给予HST(300 mg/kg)。使用定量RT-PCR检测结肠中CXCL1的mRNA水平。5-FU增强了结肠中CXCL1的mRNA,但HST及其活性成分黄芩素和6-姜酚的应用显著抑制了5-FU的这种作用。在培养的结肠组织中,5-FU处理激活了核因子κB(NF-κB),这也被HST以及黄芩素和6-姜酚的组合所抑制。此外,HST减少了5-FU诱导的腹泻发展。在这种实验条件下,HST减弱了5-FU在结肠中诱导的CXCL1基因、中性粒细胞弹性蛋白酶和髓过氧化物酶蛋白水平的上调。这些发现表明,HST,尤其是黄芩素和6-姜酚,通过抑制NF-κB活性来预防中性粒细胞募集和腹泻的发展。