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Does hepatocellular injury in sepsis involve apoptosis?
A Ayala1, T A Evans, I H Chaudry
1Center for Surgical Research, Brown University School of Medicine, Providence, Rhode Island, USA.
The Journal of Surgical Research
|August 12, 1998
Summary
Apoptosis, a programmed cell death, was investigated in septic mouse livers. Results show increased apoptosis and necrosis in hepatocytes 24 hours after sepsis induction, suggesting a combined role in liver injury.
Area of Science:
- Cell Biology
- Pathology
- Immunology
Background:
- Apoptosis (AO) is programmed cell death crucial for tissue homeostasis.
- Inappropriate AO contributes to pathological states and therapeutic nonresponsiveness in sepsis.
- The role of AO in septic liver injury remains unclear.
Purpose of the Study:
- To determine if apoptosis is evident in hepatocytes of polymicrobial septic mice.
- To investigate the temporal relationship between apoptosis and necrosis in septic liver injury.
Main Methods:
- Polymicrobial sepsis induced via cecal ligation and puncture (CLP) in C3H/HeN mice.
- Hepatocytes harvested at 4h and 24h post-CLP for apoptosis and necrosis assessment.
- Apoptosis assessed by Annexin V/propidium iodide staining, cell cycle analysis, and cell death ELISA.
- Necrosis assessed by plasma glutamic pyruvic transaminase (GPT) levels and viable cell yield.
Main Results:
- Hepatocellular apoptosis indices significantly increased at 24h post-CLP.
- DNA fragmentation was detected but faint; Annexin V staining was not fully dissociated from propidium iodide.
- Hepatocellular necrosis, indicated by elevated GPT, preceded the induction of apoptosis indices.
Conclusions:
- Both necrosis and apoptosis play a role in hepatocellular injury during polymicrobial sepsis.
- This combined cell death pattern may be unique to septic liver conditions.
- Findings suggest a complex interplay of cell death mechanisms in sepsis-induced organ dysfunction.