PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28962340-7	2015	Significant increase was observed in TUNEL positive cells and Bax (pro-apoptotic protein) expression in hippocampal sub-regions of iAs alone treated groups, whereas Bcl-2 expression was intensified in animals receiving ALA with iAs.	Thioctic Acid	219-222	BCL2, apoptosis regulator	Rattus norvegicus	165-170	
32825436-11	2020	CONCLUSION: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2.	Thioctic Acid	12-15	BCL2, apoptosis regulator	Rattus norvegicus	233-238	
26055972-6	2015	Furthermore, the level of malondialdehyde and glutathione peroxidase activity were restored, while Bcl-2-associated X protein translocation to mitochondria and cytochrome c release into the cytosol were reduced by ALA treatment.	Thioctic Acid	214-217	BCL2, apoptosis regulator	Rattus norvegicus	99-104	
33883914-14	2021	AS-IV and ALA up-regulated the expression of SIRT1 and down-regulated the expression of acetyl-p53, Drp1 and the ratio of BAX to BCL-2.	Thioctic Acid	10-13	BCL2, apoptosis regulator	Rattus norvegicus	129-134	
30605698-10	2019	Importantly, alpha-LA inhibited the activation of the ER stress eIF2alpha-ATF4 pathway, the increase of the Bax/Bcl-2 ratio, the activation of caspase-12 and -3, and the apoptosis induced by Cd.	Thioctic Acid	13-21	BCL2, apoptosis regulator	Rattus norvegicus	112-117	
30605698-11	2019	In vivo, we also found that the administration of alpha-LA alleviated Cd-induced neuronal injury, inhibited the activation of the ER stress eIF2alpha-ATF4 pathway, restored the Bax/Bcl-2 ratio, and prevented the activation of caspase-12 and -3.	Thioctic Acid	50-58	BCL2, apoptosis regulator	Rattus norvegicus	181-186	
29663489-13	2018	ALA inhibited the expression of cleaved caspase-3, cleaved caspase-9, Bax, and cytochrome c but enhanced the expression of Bcl-2.	Thioctic Acid	0-3	BCL2, apoptosis regulator	Rattus norvegicus	123-128	
28962340-8	2015	Densitometric analysis (Western blots) revealed optimal restoration of Bax and Bcl-2 ratio in animals receiving ALA with iAs, thereby suggesting the protective role of ALA in iAs induced developmental neurotoxicity.	Thioctic Acid	112-115	BCL2, apoptosis regulator	Rattus norvegicus	79-84	
28962340-8	2015	Densitometric analysis (Western blots) revealed optimal restoration of Bax and Bcl-2 ratio in animals receiving ALA with iAs, thereby suggesting the protective role of ALA in iAs induced developmental neurotoxicity.	Thioctic Acid	168-171	BCL2, apoptosis regulator	Rattus norvegicus	79-84	
21590646-10	2011	LY294002 and wortmannin decreased cell viability, and increased CHOP and Bax protein levels, and decreased Bcl-2 protein levels in ALA-pretreated and TN-treated cells.	Thioctic Acid	131-134	BCL2, apoptosis regulator	Rattus norvegicus	107-112	
23675004-2	2006	We have shown previously that supplementation of vitamin E and alpha-lipoic acid increases cardiac performance during post-ischemia reperfusion in older rats and increases Bcl-2 levels in endothelial cells.	Thioctic Acid	63-80	BCL2, apoptosis regulator	Rattus norvegicus	172-177	
15733904-0	2005	Bcl-2 in endothelial cells is increased by vitamin E and alpha-lipoic acid supplementation but not exercise training.	Thioctic Acid	57-74	BCL2, apoptosis regulator	Rattus norvegicus	0-5	
15733904-12	2005	In summary, vitamin E and alpha-lipoic acid increase endothelial cell Bcl-2, which may provide increased protection against apoptosis.	Thioctic Acid	26-43	BCL2, apoptosis regulator	Rattus norvegicus	70-75	
15662549-12	2004	Antioxidative treatment with lipoic acid significantly suppressed apoptosis and down-regulated caspase-6, -8 and -9 activity, as well as expression levels of pro-apoptotic Bcl-2 proteins without changing blood glucose levels.	Thioctic Acid	29-40	BCL2, apoptosis regulator	Rattus norvegicus	172-177