Honokiol alleviates sepsis-associated cardiac dysfunction via attenuating inflammation, apoptosis and oxidative stress

Abstract

Objective Honokiol, a natural active compound extracted from Chinese herbal medicine, can ameliorate acute lung and kidney injury of sepsis. This study was to explore the effects of honokiol on sepsis-associated cardiac dysfunction and the underlying mechanism. Methods Septic mice were induced by cecal ligation and puncture (CLP) or lipopolysaccharide (LPS), and septic HL-1 or AC16 cells were induced by LPS. Results Honokiol improved the survival and alleviated cardiac dysfunction in mice with CLP-induced sepsis. Honokiol inhibited the increased interleukin (IL) 1-β, IL-6 and tumour necrosis factor (TNF)-α in the serum and heart of CLP- and LSP-induced septic mice. Honokiol treatment reversed the increased levels of IL1-β, IL-6 and TNF-α in LPS-induced HL-1 cells. Honokiol treatment also decreased the elevated levels of IL1-β, IL-6 and TNF-α in LPS-induced AC16 cells. The increased cardiac apoptosis in CLP- and LPS-induced septic mice was alleviated by honokiol. The enhancement of oxidative stress in the heart of CLP- and LPS-induced septic mice was suppressed after honokiol administration. Conclusion These results showed that honokiol could ameliorate sepsis-associated cardiac dysfunction via attenuating inflammation, apoptosis, and oxidative stress. Honokiol is a prospective drug for sepsis-associated heart damage in the future.

Golgi Protein 73 Promotes LPS-Induced Cardiac Dysfunction via Mediating Myocardial Apoptosis and Autophagy

“…40 Increasing pieces of evidence demonstrated that cardiomyocyte apoptosis is involved in the pathogenesis of sepsis-induced cardiac dysfunction and inhibiting apoptosis could improve cardiac function. [41][42][43][44] Bcl-2 regulates the mitochondrial pathway of apoptosis, also known as intrinsic apoptosis pathway. 45 Bcl-2 was proved to protect cells against programmed cell death.…”

Apelin ameliorates sepsis-induced myocardial dysfunction via inhibition of NLRP3-mediated pyroptosis of cardiomyocytes

“…Although our study has several promising findings, several limitations should be acknowledged. First, There is mounting evidence that overproduction of ROS plays a critical role in the regulation of SMD [ 48 , 49 ]. Although we showed that NLRP3 mediated pyroptosis and inflammation contribute to SMD in the current study, whether Apelin attenuates SMD via regulation of ROS production warrants investigation.…”