PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29772867-8	2018	As for the Bcl-2 protein expression, black control group has a level of 0.081+-0.003;7 d and 14 d postoperatively, the level in Licl group was 0.151+-0.003, 0.163+-0.003 and in NS group, 0.143+-0.003, 0.154+-0.002, respectively.	Lithium Chloride	128-132	BCL2, apoptosis regulator	Rattus norvegicus	11-16	
29772867-9	2018	Licl group showed significantly increased Bcl-2 protein expression(P<0.05).	Lithium Chloride	0-4	BCL2, apoptosis regulator	Rattus norvegicus	42-47	
29772867-14	2018	CONCLUSIONS: Licl can promote the Bcl-2 protein expression and inhibit the Bax proteins expression in nerve cells of rat after SCI, thereby playing a role in the inhibition of nerve cell apoptosis.	Lithium Chloride	13-17	BCL2, apoptosis regulator	Rattus norvegicus	34-39	
30336136-6	2018	Our results showed lithium chloride inhibited glycogen synthase kinase-3beta activation, which on one hand, suppressed downstream CRMP-2/NR2B, thus diminishing the excitotoxic index level; and on the other, stabilized beta-catenin, thus modulating its downstream apoptosis-related factors such as NF-kappaB, Bcl-2 and Bax.	Lithium Chloride	19-35	BCL2, apoptosis regulator	Rattus norvegicus	308-313	
28511952-5	2017	Furthermore, we also observed that LiCl treatment significantly ameliorated the increase expression level of apoptotic neurodegeneration protein markers Bax/Bcl2, activated caspase-3 and poly (ADP-ribose) polymerase-1 (PARP-1) in the cortex and hippocampus regions of the LPS-treated adult rat brain.	Lithium Chloride	35-39	BCL2, apoptosis regulator	Rattus norvegicus	157-161	
18976035-13	2008	In the present study, 72-hour preincubation of PC12 cells with 1.2 mM lithium chloride reversed the effects of morphine on the mRNA expression of BAX and BCL-2.	Lithium Chloride	70-86	BCL2, apoptosis regulator	Rattus norvegicus	154-159	
15307905-10	2004	Immunoblotting and immunohistochemical analysis revealed that LiCl induced the expression of inactive GSK-3beta as well as the upregulation of Bcl-2 in injured RST neurons.	Lithium Chloride	62-66	BCL2, apoptosis regulator	Rattus norvegicus	143-148	
15307905-11	2004	These results indicate that in vivo, LiCl inhibits GSK-3beta and reinforces the regeneration-promoting function of ChABC through a Bcl-2-dependent mechanism.	Lithium Chloride	37-41	BCL2, apoptosis regulator	Rattus norvegicus	131-136