LI Yuanbin, YANG Jianmeng, FANG Ruoming, et al. Effects of Qi-Benefiting Phlegm-Eliminating Formula on GRP78 /BIP and Caspase-12 in Lung Cancer Xenografts Model Mice[J]. Journal of Traditional Chinese Medicine2014, 55(11): 955-958.
LI Yuanbin, YANG Jianmeng, FANG Ruoming, et al. Effects of Qi-Benefiting Phlegm-Eliminating Formula on GRP78 /BIP and Caspase-12 in Lung Cancer Xenografts Model Mice[J]. Journal of Traditional Chinese Medicine2014, 55(11): 955-958.DOI: 10.13288/j.11-2166/r.2014.11.015.
Effects of Qi-Benefiting Phlegm-Eliminating Formula on GRP78 /BIP and Caspase-12 in Lung Cancer Xenografts Model Mice
Objective To research the possible mechanism of Qi-Benefiting Phlegm-Eliminating Formula( QBPEF) for lung cancer. Methods Fifteen BALB/c mice were selected to establish lung cancer xenografts models with human lung adenocarcinoma cell A549
and the mice were randomized into model group
QBPEF low-dose group and QBPEF high-dose groups
with 5 in each. The QBPEF low-dose and high-dose groups were given 27. 3 g /( kg·d) or 54. 6g/( kg·d) crude drug of QBPEF each day respectively from the 8th day after modeling for 2 consecutive weeks. The model group was given the same volume of normal saline. The morphological changes in transplanted tumor tissue were observed with HE staining and transmission electron microscopy. The expressions of GRP78 / BIP and caspase-12 were detected with immunohistochemistry and Western blotting. The pathological changes in major organs were observed with HE staining. Results The transplanted tumor cells showed a morphological change of apoptosis in QBPEF groups after treatment
especially in the QBPEF high-dose group. Comparing with the model group
the expression of GRP78 / BIP was significantly decreased but the expressions of caspase-12 and cleaved caspase-12 were significantly increased in QBPEF groups( P < 0. 05 or P < 0. 01)
especially in the QBPEF highdose group( P < 0. 01). There was no obvious morphological change in major organs. Conclusion QBPEF can induce apoptosis in lung cancer cells with a dose-dependent manner
which may be related to activating caspase-12 and starting the endoplasmic reticulum stress apoptosis pathway.
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