Abstract
In this study, the effect of lotus leaf flavonoids (LLF) on carbon tetrachloride (CCl4)-induced liver injury in mice was studied. CCl4 was injected intraperitoneally to induce liver injury in Kunming mice. Mice were treated with LLF by gavage, and the mRNA expression levels in serum and liver were detected. Compared with the model group, LLF significantly reduced the liver index and serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), and total cholesterol (TC) levels in mice with CCl4-induced liver injury. Pathological observation showed that LLF effectively reduced morphological incompleteness and hepatocyte necrosis in CCl4-treated liver tissue. The result of quantitative polymerase chain reaction (qPCR) indicated that LLF significantly up-regulated the mRNA expression levels of copper/zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD), and catalase (CAT) and down- regulated the expression levels of tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), and interleukin-1β (IL-1β) (p < 0.05). Thus, LLF is an active ingredient that ameliorates liver injury, and it has good application prospect.
Highlights
The liver is an important organ in metabolism and physiology, and liver injury causes serious harm to the body
This study has shown that Lotus Leaf Flavonoids (LLF) can reduce the liver index of mice with liver injury, the reducing ability of high-dose LLF was significantly higher than that of low-dose LLF (p < 0.05), and the effect is similar to that of silymarin
The results of this study showed that LLF can improve liver injury induced by CCl4 in mice
Summary
The liver is an important organ in metabolism and physiology, and liver injury causes serious harm to the body. When carbon tetrachloride enters the animal body, it can directly enter the hepatocyte, and dissolve the lipid of mitochondrial membrane, it affects the structure and function of mitochondria, reduces the synthesis of enzyme protein, and causes the destruction and release of enzymes, affecting the generation of metabolism and energy, and making the hepatocyte degenerate and necrotic. Using this animal model, we can observe the metabolic disorders of sugar, fat, protein and pigment, the decrease of liver detoxification function, and the morphological changes of malnutrition, fatty. It would lead to acute liver failure and life-threatening states [4,5]
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