Introduction: Sepsis mortality rate in Indonesia reaches over 50 %, hence, acknowledgement of its pathophysiology need to be elucidated, including the pathway of apoptotic. The objective of this study was to describe the lipopolysaccharide (LPS)-induced sepsis in which triggers intrinsic apoptotic pathways in terms of the expression of caspase-9 (Cas9) and caspase-3 (Cas3).
Method: By experimental with time series randomized post test-only control group design, 48 Balb/C mice divided into 2 groups (control and treatment). Each group was injected intra-peritoneally with saline 250 ÂµL/mice and saline 250 ÂµL + 0.1 mg E. coli LPS/mice. Each group divided into 4 termination time (12th, 24th, 36th and 48th hours), examined by immunohistochemistry (IHC) for Cas9 and Cas3 expression, and analyzed by mean difference test (Mann-Whitney and t test) and correlation test (Spearmanâ€™s test).
Results: The LPS-induced sepsis in the treatment group revealed increasing number of caspase-9 compared to control group (2.34+0.24 vs 0.82+0.08; p<0.001. There were increasing trends in the treatment group compared to control group includes for: all groups Cas3 (1.54+0.10 vs 0.48+0.05; p<0.001), t12 Cas3 (3.25+0.22 vs 0.50+0.06; p<0.001), t24 Cas3 (1.37+0.27 vs 0.45+0.05; p=0,002), and t36 Cas3 (1.03+0.20 vs 0.52+0.22; p=0,002). Instead, there were no difference between treatment group and control group for t48 Cas3 (0.50+0.14 vs 0.43+0.10; p=0,485). There was decreasing pattern on serial time 12, 24, 36 and 48 hours for Cas9 (p<0,001) and Cas3 (p=0,002). There was a correlation between Cas9-Cas3 (rs=0.835;p=0.001).
Conclusion: The LPS-induced sepsis caused an increase of caspase-9 and caspase-3, strongly correlated with decreasing pattern on time serial.