Sakagami Hiroshi, Tsuji Mayumi, Tomomura Mineko, Masuda Yoshiko, Iwama Soichi, Nakagawa Mika, Suzuki Hayato, Tanaka Kenta, Abe Tomoyuki, Tamura Nobuaki, Tomomura Akito, Yokose Satoshi, Takeshima Hiroshi, Natori Takenori, Horiuchi Misaki, Fujisawa Tomohiro, Kiuchi Yuji, Oguchi Katsuji, Yasui Toshikazu, Oizumi Hiroshi, Oizumi Takaaki
Meikai University School of Dentistry, Saitama, Japan
School of Medicine, Showa University, Tokyo, Japan.
In Vivo. 2018 Mar-Apr;32(2):231-239. doi: 10.21873/invivo.11229.
BACKGROUND/AIM: We have previously reported the protection of doxorubicin-induced keratinocyte toxicity by alkaline extract of the leaves of Sasa senanensis Rehder (SE). In order to extend the generality of the cell protective effect of SE, we investigated whether it also protects rat PC12 and human SH-SY5Y neuron model cells from amyloid β-peptide (Aβ)-induced injury.
Viability of cells was determined by the MTT method. Cytotoxicity was evaluated by the concentration that reduces the cell viability by 50% (CC). Protection from Aβ-induced cytotoxicity was evaluated by the concentration that reversed the Aβ-induced reduction of viability by 50% (EC). The selectivity index (SI) of neuroprotective activity was defined as the ratio of EC to CC Aβ aggregation was assayed using Aβ ammonium hydroxide.
SE showed hormetic growth stimulation at lower concentrations in both neuron precursors and differentiated cells. SE reproducibly inhibited Aβ-induced cytotoxicity against both undifferentiated and differentiated neuron cells. Both the extent of differentiation induction and viability depended on the cell density, suggesting the release of growth and differentiation stimulation substances into culture supernatant. Higher concentrations of SE partially reduced the Aβ aggregation.
Hormetic growth stimulation and inhibition of aggregation may be involved in the neuroprotective activity of SE.
背景/目的：我们之前报道了青篱竹（Sasa senanensis Rehder）叶的碱性提取物（SE）对阿霉素诱导的角质形成细胞毒性具有保护作用。为了扩展SE细胞保护作用的普遍性，我们研究了它是否也能保护大鼠PC12和人SH-SY5Y神经元模型细胞免受淀粉样β肽（Aβ）诱导的损伤。
采用MTT法测定细胞活力。通过使细胞活力降低50%的浓度（CC）评估细胞毒性。通过使Aβ诱导的活力降低逆转50%的浓度（EC）评估对Aβ诱导的细胞毒性的保护作用。神经保护活性的选择性指数（SI）定义为EC与CC的比值。使用氢氧化铵Aβ测定Aβ聚集情况。
在较低浓度下，SE在神经元前体细胞和分化细胞中均表现出兴奋性生长刺激作用。SE可重复性地抑制Aβ对未分化和分化神经元细胞的细胞毒性。分化诱导程度和活力均取决于细胞密度，提示生长和分化刺激物质释放到培养上清液中。较高浓度的SE部分降低了Aβ聚集。
兴奋性生长刺激和聚集抑制可能参与了SE的神经保护活性。
