Journal of ethnopharmacology · 2025
Sphingoid bases extracted from Hippocampus trimaculatus Leach induces apoptosis in human leukemia K562 cells through the mitochondria-dependent pathway.
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Lu Yuehan, Zhao Mantong, Lin Hongping, Xia Guanghua, Li Chuan, Zhou Dayong, Liu Zhongyuan
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Hippocampus trimaculatus is an important traditional Chinese medicine, which has been used to warm and tonify kidney yang in the clinic for a long time. Modern studies have also shown that it can also display various pharmacological activities such as anti-inflammation and antitumor due to the abundant ingredients. However, its therapeutic effect and mechanism against tumors like leukemia, which emerge as a prevalent type of hematological tumor disease, requires further research.
AIM OF THE STUDY: The current study aimed to investigate the therapeutic effect of sphingoid bases extracted from Hippocampus trimaculatus Leach against human chronic myeloid leukemia K562 cells through mitochondria-dependent apoptotic pathway.
MATERIALS AND METHODS: The sphingoid bases extracted from Hippocampus trimaculatus Leach (SBHTL) was determined by Fourier transform infrared spectroscopy (FTIR) and gas chromatography-mass spectrometry (GC-MS). Human chronic myeloid leukemia K562 cells was treated with different concentrations of SBHTL. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis was assessed by flow cytometry, Annexin V assay. The mitochondrial membrane potential was detected by fluorescence intensity with probe Rhodamine 123. Cell cycle was analyzed by the MuseTM Cell Cycle Kit. Real-time quantitative polymerase chain reaction and western blot analysis were used to detect anti-apoptotic B cell lymphoma/leukemia-2 (Bcl-2), pro-apoptotic Bcl-2-associated X (Bax), caspase-3, caspase-9 expressions.
RESULTS: The SBHTL species mainly consist of d16:0, d18:2 and d20:2 based on the determination by GC-MS and FTIR, which barely exist in mammals. SBHTL significantly induced apoptosis of human chronic myeloid leukemia K562 cells in a dose-dependent manner. Moreover, the SBHTL could cause mitochondrial membrane potential loss of K562 cells and down-regulate the Bcl-2, up-regulate the Bax as well as subsequently active the expression of caspase-3, 8, and 9. In conclusion, SBHTL could induce apoptosis in the K562 cells via the mitochondria-dependent pathways.
CONCLUSION: SBHTL could induce apoptosis in the K562 cells via the mitochondria-dependent pathways. They exerted great potential efficacy for the treatment of tumors like leukemia.
AIM OF THE STUDY: The current study aimed to investigate the therapeutic effect of sphingoid bases extracted from Hippocampus trimaculatus Leach against human chronic myeloid leukemia K562 cells through mitochondria-dependent apoptotic pathway.
MATERIALS AND METHODS: The sphingoid bases extracted from Hippocampus trimaculatus Leach (SBHTL) was determined by Fourier transform infrared spectroscopy (FTIR) and gas chromatography-mass spectrometry (GC-MS). Human chronic myeloid leukemia K562 cells was treated with different concentrations of SBHTL. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis was assessed by flow cytometry, Annexin V assay. The mitochondrial membrane potential was detected by fluorescence intensity with probe Rhodamine 123. Cell cycle was analyzed by the MuseTM Cell Cycle Kit. Real-time quantitative polymerase chain reaction and western blot analysis were used to detect anti-apoptotic B cell lymphoma/leukemia-2 (Bcl-2), pro-apoptotic Bcl-2-associated X (Bax), caspase-3, caspase-9 expressions.
RESULTS: The SBHTL species mainly consist of d16:0, d18:2 and d20:2 based on the determination by GC-MS and FTIR, which barely exist in mammals. SBHTL significantly induced apoptosis of human chronic myeloid leukemia K562 cells in a dose-dependent manner. Moreover, the SBHTL could cause mitochondrial membrane potential loss of K562 cells and down-regulate the Bcl-2, up-regulate the Bax as well as subsequently active the expression of caspase-3, 8, and 9. In conclusion, SBHTL could induce apoptosis in the K562 cells via the mitochondria-dependent pathways.
CONCLUSION: SBHTL could induce apoptosis in the K562 cells via the mitochondria-dependent pathways. They exerted great potential efficacy for the treatment of tumors like leukemia.