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[Nitric oxide mediated TNF-α, IL-1β gene expression in liver induced by crush injury of rat's soft tissues]
Objective:
To explore the effect of nitric oxide (NO) on the gene expression of hepatic TNF-α and IL-1β by crush injury of rat's soft tissues.
Methods:
Rats were randomly divided into sham group, crush group, crush+aminoguanidine (AG) group, and crush+L-arginine (L-Arg) group. Activities of ALT and AST as well as NO level in serum were measured. Gene expressions of TNF-α and IL-1β were detected with RT-PCR.
Results:
Obvious increase in TNF-α and IL-1β mRNA expression was detected in the crush group compared with the sham group (P<0.05). After pretreated L-Arg, expressions of TNF-α and IL-1β mRNA were markedly increased (P<0.05). After pretreated AG, those indices obviously decreased (P<0.05). Activities of ALT and AST enhanced and NO level increased in the crush group compared with the sham group (P<0.05). Pretreatment with L-Arg or AG led to substantial increased or reduced activities of ALT and AST as well as NO levels, respectively.
Conclusion:
Endogenous NO mediated TNF-α, IL-1β mRNA up expression in liver induced by increased production of NO after crush injury of rat's soft tissues.
Insights
Crush injury in rats increases liver nitric oxide (NO), leading to higher expression of TNF-α and IL-1β. This suggests endogenous NO plays a key role in the inflammatory response following soft tissue trauma.
Area of Science:
- Biochemistry
- Molecular Biology
- Physiology
Background:
- Crush injury can trigger systemic inflammatory responses.
- Nitric oxide (NO) is a critical signaling molecule involved in inflammation and tissue repair.
- Tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) are key pro-inflammatory cytokines.
Purpose of the Study:
- To investigate the role of endogenous nitric oxide (NO) in regulating the gene expression of hepatic TNF-α and IL-1β following soft tissue crush injury in rats.
- To determine how modulating NO levels affects inflammatory markers in the liver after trauma.
Main Methods:
- Rats were subjected to soft tissue crush injury and divided into groups: sham, crush, crush with aminoguanidine (NO inhibitor), and crush with L-arginine (NO precursor).
- Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and NO were measured.
- Hepatic gene expression of TNF-α and IL-1β was quantified using reverse transcription-polymerase chain reaction (RT-PCR).
Main Results:
- Crush injury significantly increased hepatic mRNA expression of TNF-α and IL-1β compared to the sham group (P<0.05).
- Administration of L-arginine further elevated TNF-α and IL-1β mRNA levels, while aminoguanidine significantly reduced them (P<0.05).
- Crush injury elevated ALT, AST, and serum NO levels, which were modulated by L-arginine and aminoguanidine treatments.
Conclusions:
- Endogenous nitric oxide (NO) significantly mediates the upregulation of TNF-α and IL-1β gene expression in the liver following soft tissue crush injury.
- Increased NO production post-trauma appears to drive the hepatic inflammatory response.
- Modulating NO levels could be a potential therapeutic strategy for managing inflammation after crush injuries.
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