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Open Access Issue
Protective Effect of Lyophyllum ulmarium Fibrinolytic Enzyme on Vascular Intima in Rats with Arterial Thrombosis
Rihua CUI, Yu LI, Xin SU, Ying WEI, Jiarui CHEN, Minghua SHEN
Food Science 2022, 43(15): 134-140
Published: 15 August 2022
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Objective

To study the protective effect of Lyophyllum ulmarium fibrinolytic enzyme (LUFE) on intimal injury during arterial thrombosis in rats.

Methods

Fifty SD rats were randomly divided into five groups: sham operation, model, aspirin, and low- and high-dose LUFE. Before the model establishment, the rats in the aspirin and LUFE groups were administrated with 10 mg/kg mb of aspirin, and 100 and 400 mg/kg mb of LUFE, respectively, by gavage for seven consecutive days. On the following day, the rats in all groups except the sham operation group were administered with ferric chloride to induce carotid artery thrombosis. The morphological changes of carotid artery were observed by HE staining.The serum levels of C-reactive protein (CRP), interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), intercellular cell adhesion molecule-1 (ICAM-1), and platelet endothelial cell adhesion molecule-1 (PECAM-1) were detected by an enzyme-linked immunosorbent assay. The level of platelet-leukocyte aggregates (PLA) was detected by flow cytometry. The adhesion of platelets to solidified collagen was observed in vitro after LUFE intervention. The level of Ca2+ in platelets stimulated by collagen was detected by flow cytometry. The phosphorylation levels of platelet linker for activation of T cells (LAT) and phospholipase Cγ (PLCγ) were detected by Western blot.

Results

LUFE intervention significantly reduced vascular intimal injury, lowered the levels of serum CPR, IL-6, IL-8, MCP-1, ICAM-1 and PECAM-1 in different degrees, and decreased the level of PLA. LUFE reduced in vitro platelet adhesion to collagen, decreased platelet Ca2+ level, and down-regulated the phosphorylation of platelet LAT and PLCγ proteins.

Conclusion

LUFE inhibits vascular inflammation during thrombosis, which may be related to the protective effect on vascular endothelial cells and the antiplatelet effect of LUFE.
Open Access Issue
Protective Effects of Armillaria mellea Polysaccharides against Ethanol-Induced Vascular Endothelial Cell Injury in Rats
Junhui ZHANG, Ranran CHEN, He CONG, Minghua SHEN
Food Science 2024, 45(7): 127-134
Published: 15 April 2024
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The aim of this study is to evaluate the protective effect of Armillaria mellea polysaccharides (AMP) against ethanol-induced vascular endothelial cell injury in rats. Altogether 40 SD rats were randomly divided into 4 groups: normal control, injury, low-and high-dose AMP. The rats from all groups except the normal control group were gavaged with 40% ethanol at 10 mL/kg mb to induce endothelial cell injury. The rats in the low-and high-dose groups were gavaged with AMP at 100 and 400 mg/kg mb, respectively, while the remaining groups were given an equal volume of physiological saline. The administration period lasted for 4 weeks. The histopathological changes of carotid arteries were observed by hematoxylin-eosin (HE) staining. Serum triglycerides (TG), total cholesterol (T-CHO), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitric oxide (NO), endothelin 1 (ET-1), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were detected. In addition, the effects of different doses (100 and 400 μg/mL) of AMP on the levels of reactive oxygen species (ROS), mitochondrial transmembrane potential, apoptosis, and the expression of apoptosis-associated proteins such as B cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), and caspase-3 in human umbilical vein endothelial cell injured by 600 μmol/mL ethanol were investigated. Results: AMP attenuated ethanol-induced endothelial cell injury, decreased T-CHO, TG, LDL-C, iNOS, NO, ET-1, and MDA levels, and increased HDL-C and SOD activity. In vitro, AMP reduced cellular ROS levels, inhibited the ethanol-induced decrease in mitochondrial transmembrane potential and apoptosis, increased Bcl-2/Bax ratio and down-regulated the expression of cleaved caspase-3. Conclusion: AMP have a protective effect against ethanol-induced endothelial cell injury in rats, and the mechanism may be related to their lipid-lowering, antioxidant, and anti-apoptotic effects.

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