PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
6533413-1	1984	The effect of oral administration of the pyrrolizidine alkaloids, seneciphylline and senecionine, from Senecio vulgaris (Compositae) on activities of hepatic epoxide hydrase, glutathione-S-transferase, aminopyrine-N-demethylase and arylhydrocarbon hydroxylase (AHH) was investigated in microsomes of young male albino rats.	seneciphylline	66-80	hematopoietic prostaglandin D synthase	Rattus norvegicus	175-200
6533413-1	1984	The effect of oral administration of the pyrrolizidine alkaloids, seneciphylline and senecionine, from Senecio vulgaris (Compositae) on activities of hepatic epoxide hydrase, glutathione-S-transferase, aminopyrine-N-demethylase and arylhydrocarbon hydroxylase (AHH) was investigated in microsomes of young male albino rats.	seneciphylline	66-80	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	261-264
6533413-2	1984	Seneciphylline significantly increased the activities of epoxide hydrase and glutathione-S-transferase but caused reduction of cytochrome P-450 and related monooxygenase activities.	seneciphylline	0-14	hematopoietic prostaglandin D synthase	Rattus norvegicus	77-102
6533413-2	1984	Seneciphylline significantly increased the activities of epoxide hydrase and glutathione-S-transferase but caused reduction of cytochrome P-450 and related monooxygenase activities.	seneciphylline	0-14	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	127-143
33886121-10	2021	The results revealed that seneciphylline was quickly absorbed into plasma (Tmax 0.23-0.32 h) and reached the max concentration of 0.82-1.75 mug/mL after oral administration.	seneciphylline	26-40	thrombopoietin	Mus musculus	144-146
32618019-6	2020	Further research uncovered that Seph induced apoptosis by disrupting mitochondrial homeostasis, inducing mitochondrial depolarization, mitochondrial membrane potential (MMP) loss, and cytochrome c (Cyt c) release and activating c-Jun N-terminal kinase (JNK).	seneciphylline	32-36	mitogen-activated protein kinase 8	Mus musculus	228-251
32618019-6	2020	Further research uncovered that Seph induced apoptosis by disrupting mitochondrial homeostasis, inducing mitochondrial depolarization, mitochondrial membrane potential (MMP) loss, and cytochrome c (Cyt c) release and activating c-Jun N-terminal kinase (JNK).	seneciphylline	32-36	mitogen-activated protein kinase 8	Mus musculus	253-256
32618019-7	2020	The Seph-induced apoptosis in hepatocytes could be alleviated by Mdivi-1 (50 muM, a dynamin-related protein 1 inhibitor), as well as SP600125 (25 muM, a specific JNK inhibitor) and ZVAD-fmk (50 muM, a general caspase inhibitor).	seneciphylline	4-8	dynamin 1-like	Mus musculus	84-109
32618019-7	2020	The Seph-induced apoptosis in hepatocytes could be alleviated by Mdivi-1 (50 muM, a dynamin-related protein 1 inhibitor), as well as SP600125 (25 muM, a specific JNK inhibitor) and ZVAD-fmk (50 muM, a general caspase inhibitor).	seneciphylline	4-8	mitogen-activated protein kinase 8	Mus musculus	162-165