Objective To investigate the role of plantamajoside in sepsis-related cardiac injury in mice.

Methods Forty male C57/BL6 mice aged 8 to 10 weeks were selected and randomly divided into 4 groups according to different treatment methods: normal saline+normal saline group, normal saline+plantamajoside group, lipopolysaccharide+normal saline group, lipopolysaccharide+plantamajoside group, with 10 mice in each group. Mice in lipopolysaccharide+normal saline group and lipopolysaccharide+plantamajoside group received single intraperitoneal injection of lipopolysaccharide (10 mg/kg) to construct a mouse sepsis model; mice in the normal saline+normal saline group and the normal saline+plantamajoside group received intraperitoneal injection of the same volume of normal saline. The mice in the normal saline+plantamajoside group and the lipopolysaccharide+plantamajoside group were given 50 mg/(kg·d) plantamajoside by gavage intervention for consecutive 5 days, and the mice in the normal saline+normal saline group and the lipopolysaccharide+normal saline group were given gavage with the same volume of normal saline. On the first day of the experiment, the mice were given 50 mg/(kg·d) or normal saline intragastric administration for 5 consecutive days. On the fifth day, mice were given a single intraperitoneal injection of lipopolysaccharide (10 mg/kg) or equal volume of normal saline. After feeding for 12 h, cardiac function was detected and samples were collected. Superoxide dismutase 2 (SOD-2), glutathione peroxidase-1 (GPX-1), catalase (CAT) and related inflammatory factors interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1) and interleukin-4 (IL-4) mRNA levels were determined by real-time quantitative fluorescence polymerase chain reaction. The levels of malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), GPX-1, TNF-α, MCP-1 and Caspase-3 were determined by the test kit; the serum levels of cardiac troponin I (cTnI) and lactate dehydrogenase (LDH) were detected; the myocardial cell apoptosis was detected by TUNEL staining.

Results Compared with normal saline + normal saline group, the heart rate, left ventricular ejection fraction and left ventricular short axis shortening rate of mice in lipopolysaccharide + normal saline group were significantly decreased, and the myocardial injury markers including cTnI and LDH were significantly increased (P < 0.05). Plantamajoside could restore the heart rate, left ventricular ejection fraction, left ventricular short axis shortening rate, reduce the levels of myocardial injury markers including cTnI and LDH, and improve the survival rate of mice (P < 0.05). Compared with the lipopolysaccharide+normal saline group, the levels of MDA and 4-HNE in the heart of mice in lipopolysaccharide+plantamajoside group were significantly decreased (P < 0.05). Plantamajoside could decrease the expression of inflammatory factors, the activity of Caspase-3 and the level of apoptosis in the heart of mice (P < 0.05).

Conclusion Plantamajoside can alleviate myocardial cell damage induced by lipopolysaccharide and improve cardiac function in mice.