PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30575685-4	2019	Because TXA does not block uPA-dependent plasmin generation from PLG and instead augments it, we hypothesized that administration of TXA could enhance or inhibit proinflammatory C5a formation in a PLG activator-dependent manner.	Tranexamic Acid	133-136	complement C5a receptor 1	Homo sapiens	178-181	
30575685-10	2019	RESULTS: Plasmin-mediated fibrinolysis by tPA in clotted PPP led to an approximately threefold increase in C5a production (p < 0.0001), which was significantly inhibited by TXA (p < 0.001).	Tranexamic Acid	173-176	complement C5a receptor 1	Homo sapiens	107-110	
30575685-11	2019	Paradoxically, when fibrinolysis was induced by uPA, TXA treatment led to further increases in C5a production beyond uPA alone (p < 0.0001).	Tranexamic Acid	53-56	complement C5a receptor 1	Homo sapiens	95-98	
30575685-14	2019	CONCLUSIONS: Tranexamic acid administration can have proinflammatory or anti-inflammatory effects through regulating C5a generation by plasmin, depending on the predominating PLG activator.	Tranexamic Acid	13-28	complement C5a receptor 1	Homo sapiens	117-120	
30575685-15	2019	Tranexamic acid may cause significant inflammatory C5a elevations in injured tissues by augmenting uPA-mediated plasmin generation in a fibrin-independent manner.	Tranexamic Acid	0-15	complement C5a receptor 1	Homo sapiens	51-54	
30575685-16	2019	In contrast, TXA reduces C5a generation during tPA-mediated fibrinolysis that may reduce inflammatory responses.	Tranexamic Acid	13-16	complement C5a receptor 1	Homo sapiens	25-28