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Updated: May 30, 2026
Use of Animal Model of Sepsis to Evaluate Novel Herbal Therapies
Published on: April 11, 2012
Myrrh inhibits LPS-induced inflammatory response and protects from cecal ligation and puncture-induced sepsis
Min-Sun Kim1, Gi-Sang Bae, Kyoung-Chel Park
1Department of Herbology, School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 540-749, Republic of Korea.
Abstract:
Myrrh has been used as an antibacterial and anti-inflammatory agent. However, effect of myrrh on peritoneal macrophages and clinically relevant models of septic shock, such as cecal ligation and puncture (CLP), is not well understood. Here, we investigated the inhibitory effect and mechanism(s) of myrrh on inflammatory responses. Myrrh inhibited LPS-induced productions of inflammatory mediators such as nitric oxide, prostaglandin E(2), and tumor necrosis factor-α but not of interleukin (IL)-1β and IL-6 in peritoneal macrophages. In addition, Myrrh inhibited LPS-induced activation of c-jun NH(2)-terminal kinase (JNK) but not of extracellular signal-regulated kinase (ERK), p38, and nuclear factor-κB. Administration of Myrrh reduced the CLP-induced mortality and bacterial counts and inhibited inflammatory mediators. Furthermore, administration of Myrrh attenuated CLP-induced liver damages, which were mainly evidenced by decreased infiltration of leukocytes and aspartate aminotransferase/alanine aminotransferase level. Taken together, these results provide the evidence for the anti-inflammatory and antibacterial potential of Myrrh in sepsis.
Insights
Myrrh demonstrates antibacterial and anti-inflammatory properties, reducing mortality and liver damage in sepsis models. It inhibits key inflammatory mediators and bacterial counts, highlighting its therapeutic potential.
Area of Science:
- Pharmacology
- Immunology
- Microbiology
Background:
- Myrrh is traditionally used for antibacterial and anti-inflammatory effects.
- Its impact on peritoneal macrophages and sepsis models like cecal ligation and puncture (CLP) remains unclear.
Purpose of the Study:
- To investigate the inhibitory effects and mechanisms of myrrh on inflammatory responses.
- To evaluate myrrh's efficacy in a clinically relevant model of septic shock.
Main Methods:
- Assessed myrrh's effect on lipopolysaccharide (LPS)-induced inflammatory mediators and signaling pathways (JNK, ERK, p38, NF-κB) in peritoneal macrophages.
- Administered myrrh in a cecal ligation and puncture (CLP) mouse model to evaluate mortality, bacterial counts, inflammatory mediators, and liver damage.
Main Results:
- Myrrh inhibited LPS-induced nitric oxide, prostaglandin E(2), and tumor necrosis factor-α production, and JNK activation.
- Myrrh administration reduced CLP-induced mortality, bacterial load, and liver damage (decreased leukocyte infiltration and liver enzymes).
- Myrrh did not inhibit LPS-induced IL-1β and IL-6 production or ERK, p38, and NF-κB activation.
Conclusions:
- Myrrh exhibits significant anti-inflammatory and antibacterial potential in sepsis.
- Myrrh may serve as a therapeutic agent for sepsis by modulating inflammatory responses and reducing bacterial burden.
