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Updated: Sep 25, 2025
Use of Animal Model of Sepsis to Evaluate Novel Herbal Therapies
Published on: April 11, 2012
Berberine attenuates sepsis-induced cardiac dysfunction by upregulating the Akt/eNOS pathway in mice
Hong Zhang1, Xiaofei Wu1, Yanyan Tao1
1Department of Emergency, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233030, P.R. China.
Insights
Berberine protects against sepsis-induced heart dysfunction in mice by improving cardiac function and reducing inflammation. This effect is mediated through the Akt/eNOS pathway, highlighting berberine
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Sepsis can lead to cardiac dysfunction.
- Understanding protective mechanisms is crucial for treatment.
Purpose of the Study:
- Investigate berberine's cardioprotective effects in sepsis.
- Elucidate the underlying molecular mechanisms.
Main Methods:
- Mice were induced with sepsis using lipopolysaccharide (LPS).
- Berberine was administered with or without L-NAME (an NOS inhibitor).
- Cardiac function, inflammatory markers, and oxidative stress were assessed.
Main Results:
- LPS induced cardiac dysfunction, increased inflammatory markers, and oxidative stress.
- Berberine administration improved cardiac function and reduced these markers.
- Berberine upregulated the Akt/eNOS pathway, an effect blocked by L-NAME.
Conclusions:
- Berberine exhibits cardioprotective effects against sepsis-induced cardiac dysfunction.
- The Akt/eNOS pathway is critical for berberine's beneficial actions.
- Berberine shows therapeutic potential for sepsis-related heart issues.
Abstract:
The present study aimed to investigate the cardioprotective role of berberine in sepsis-induced cardiac dysfunction and consider the underlying mechanisms. C57BL/6J mice were randomized into four groups, namely, Control, lipopolysaccharide (LPS), LPS + berberine and LPS + Nω-nitro-L-arginine methyl ester (L-NAME) + berberine. A single dose (10 mg/kg body weight) of LPS was intraperitoneally administered to mice to induce cardiac dysfunction, whereas the Control group was administered with an equivalent volume of saline. In the LPS + berberine and LPS + L-NAME + berberine group, berberine (10 mg/kg body weight) dissolved in hot water was intraperitoneally administered 30 min after the LPS treatment. In the LPS + L-NAME + berberine group, L-NAME (100 mg/kg body weight) dissolved in saline was intraperitoneally administered 30 min before the LPS treatment. Then, ~6 h after the LPS treatment, a significant decrease was observed in the left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). Meanwhile, the plasma myocardial injury markers, inflammatory factors and oxidative stress levels were significantly increased in the LPS group compared with the Control group. The administration of berberine improved the ventricular function and decreased the plasma myocardial injury markers, inflammatory factors and oxidative stress levels. In addition, it increased the heart total nitric oxide synthase (NOS) activity and upregulated the protein expressions of p-Akt and phosphorylated endothelial (e)NOS, which indicated that the Akt/eNOS pathway was activated by berberine. However, the cardioprotective effects of berberine were counteracted by L-NAME, an NOS inhibitor, which inhibited the eNOS activity. In conclusion, berberine attenuated sepsis-induced cardiac dysfunction by upregulating the Akt/eNOS pathway in mice.
