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Dl-3-n-Butylphthalide (NBP) Mitigates Muscular Injury Induced by Limb Ischemia/Reperfusion in Mice through the
Huanhuan Sun1, Jueqiong Wang2, Wei Bi1
1Department of Vascular Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, China.
Objective:
Limb ischemia/reperfusion (I/R) injury is a clinical syndrome associated with severe damages to skeletal muscles and other fatal outcomes. Oxidative stress and inflammatory response play vital roles in the development of limb I/R injury. Existing evidence further indicates that Dl-3-n-butylphthalide (NBP) has anti-inflammatory and antioxidative properties. However, whether NBP can protect skeletal muscles from limb I/R injury and the mechanism in mediating the action of NBP treatment still remain to be investigated, which are the focuses of the current study.
Methods:
The model of limb I/R injury was established and H&E staining was adopted to assess the pathological changes in skeletal muscles following limb I/R injury. Additionally, the W/D ratio of muscle tissue was also measured. ELISA and biochemical tests were carried out to measure the levels of inflammatory cytokines and oxidative stress in mouse models of limb I/R injury. Moreover, the levels of the HMGB1/TLR4/NF-κB pathway-related proteins were also determined using immunohistochemistry and immunoblotting.
Results:
It was established that NBP treatment alleviated I/R-induced pathological changes in muscular tissue of mice, accompanied by lower W/D ratio of skeletal muscular tissue. Meanwhile, the limb I/R-induced inflammation and oxidative stress in skeletal muscles of mice were also inhibited by NBP. Mechanistic study indicated that the alleviatory effect of NBP was ascribed to inactivation of the HMGB1/TLR4/NF-κB pathway.
Conclusions:
Our findings highlighted the potential of NBP as a novel strategy for limb I/R-driven muscle tissue damages by suppressing inflammatory response and oxidative stress via the HMGB1/TLR4/NF-κB pathway.
Insights
Dl-3-n-butylphthalide (NBP) protects skeletal muscles from limb ischemia/reperfusion (I/R) injury by reducing oxidative stress and inflammation. NBP achieves this by inhibiting the HMGB1/TLR4/NF-κB pathway, offering a potential new treatment strategy.
Area of Science:
- Biomedical Science
- Pharmacology
- Skeletal Muscle Physiology
Background:
- Limb ischemia/reperfusion (I/R) injury causes significant skeletal muscle damage.
- Oxidative stress and inflammation are key contributors to I/R injury pathology.
- Dl-3-n-butylphthalide (NBP) exhibits known anti-inflammatory and antioxidative properties.
Purpose of the Study:
- To investigate the protective effects of NBP on skeletal muscle against limb I/R injury.
- To elucidate the underlying molecular mechanisms of NBP's action in I/R injury.
Main Methods:
- Established a mouse model of limb I/R injury.
- Assessed pathological changes using H&E staining and measured the wet/dry (W/D) weight ratio of muscle tissue.
- Quantified inflammatory cytokines and oxidative stress markers via ELISA and biochemical assays.
- Determined levels of HMGB1/TLR4/NF-κB pathway proteins using immunohistochemistry and immunoblotting.
Main Results:
- NBP treatment significantly alleviated I/R-induced skeletal muscle damage and reduced the W/D ratio.
- NBP effectively inhibited limb I/R-induced inflammation and oxidative stress in skeletal muscles.
- Mechanistic studies revealed that NBP inactivated the HMGB1/TLR4/NF-κB signaling pathway.
Conclusions:
- NBP demonstrates significant potential as a therapeutic agent for limb I/R injury.
- NBP mitigates skeletal muscle damage by suppressing inflammation and oxidative stress.
- The protective effects of NBP are mediated through the inhibition of the HMGB1/TLR4/NF-κB pathway.
