Genistein has the function of alleviating and treating disseminated intravascular coagulation caused by lipopolysaccharide

Chen, Xueqin; Tan, Jingyi; Yang, Mengqi; Liao, Zhi-Kai; Cheng, Lü; Huang, Youwei; Wu, Li

doi:10.1007/s11418-018-1215-9

Cited by 7 publications

(4 citation statements)

References 73 publications

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“…The PT index was significantly increased after LPS infusion, indicating that the coagulation factor was greatly reduced and, consequently, the PT was prolonged. In the fibrinolysis phase induced by LPS, the body produced a large amount of fibrin degradation products, so the APTT was extended [ 42 , 43 ]. In contrast, all indexes were significantly improved, as shown by a decrease in upregulation of PT and APTT after um-PEA treatment, indicating that um-PEA has a good regulatory effect on the disorder of the coagulation and fibrinolytic system in DIC.…”

Section: Discussionmentioning

confidence: 99%

Ultramicronized Palmitoylethanolamide in the Management of Sepsis-Induced Coagulopathy and Disseminated Intravascular Coagulation

D’Amico

Monaco

Siracusa

et al. 2021

IJMS

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Disseminated intravascular coagulation (DIC) is a severe condition characterized by the systemic formation of microthrombi complicated with bleeding tendency and organ dysfunction. In the last years, it represents one of the most frequent consequences of coronavirus disease 2019 (COVID-19). The pathogenesis of DIC is complex, with cross-talk between the coagulant and inflammatory pathways. The objective of this study is to investigate the anti-inflammatory action of ultramicronized palmitoylethanolamide (um-PEA) in a lipopolysaccharide (LPS)-induced DIC model in rats. Experimental DIC was induced by continual infusion of LPS (30 mg/kg) for 4 h through the tail vein. Um-PEA (30 mg/kg) was given orally 30 min before and 1 h after the start of intravenous infusion of LPS. Results showed that um-PEA reduced alteration of coagulation markers, as well as proinflammatory cytokine release in plasma and lung samples, induced by LPS infusion. Furthermore, um-PEA also has the effect of preventing the formation of fibrin deposition and lung damage. Moreover, um-PEA was able to reduce the number of mast cells (MCs) and the release of its serine proteases, which are also necessary for SARS-CoV-2 infection. These results suggest that um-PEA could be considered as a potential therapeutic approach in the management of DIC and in clinical implications associated to coagulopathy and lung dysfunction, such as COVID-19.

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Section: Discussionmentioning

confidence: 99%

Ultramicronized Palmitoylethanolamide in the Management of Sepsis-Induced Coagulopathy and Disseminated Intravascular Coagulation

D’Amico

Monaco

Siracusa

et al. 2021

IJMS

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“…The establishment of the DIC rat model was performed in accordance with methods described in the literature [ 42 ]. The 33 rats were randomly divided into three groups ( n = 11/group), as follows: (1) control group: normal saline + normal saline; (2) LPS group: normal saline + 15 mg/kg LPS; and (3) SAA40 group: 40 mg/kg SAA + 15 mg/kg LPS.…”

Section: Methodsmentioning

confidence: 99%

Salvianolic acid A alleviates lipopolysaccharide-induced disseminated intravascular coagulation by inhibiting complement activation

Zhang

Guo

et al. 2022

BMC Complement Med Ther

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Introduction Disseminated intravascular coagulation (DIC) is a syndrome characterized by coagulopathy, microthrombus, and multiple organ failure. The complement system in DIC is overactivated, and the functions of complement and coagulation pathways are closely related. Our previous screening revealed that salvianolic acid A (SAA) has anti-complement activity. The hyper-activated complement system was involved in the lipopolysaccharide (LPS) induced DIC in rats. The effects of SAA anti-complement action on LPS-induced DIC in rats were investigated. Methods The complement activity of the classical pathway and alternative pathway was detected through an in vitro hemolysis assay. The binding sites of SAA and complement C3b were predicted by molecular docking. LPS-induced disseminated coagulation experiments were performed on male Wistar rats to assess coagulation function, complement activity, inflammation, biochemistry, blood routine, fibrinolysis, and survival. Results SAA had an anti-complement activity in vivo and in vitro and inhibited the complement activation in the classical and alternative pathway of complement. The infusion of LPS into the rats impaired the coagulation function, increased the plasma inflammatory cytokine level, complemented activation, reduced the clotting factor levels, fibrinogen, and platelets, damaged renal, liver, and lung functions, and led to a high mortality rate (85%). SAA treatment of rats inhibited complement activation and attenuated the significant increase in D-dimer, interleukin-6, alanine aminotransferase, and creatinine. It ameliorated the decrease in plasma levels of fibrinogen and platelets and reversed the decline in activity of protein C and antithrombin III. The treatment reduced kidney, liver, and lung damage, and significantly improved the survival rate of rats (46.2 and 78.6% for the low- and high-dose groups, respectively). Conclusion SAA reduced LPS-induced DIC by inhibiting complement activation. It has considerable potential in DIC treatment.

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“…For example, an animal experiment showed that genistein pretreatment (10 mg/kg) dramatically suppressed fractalkine expression through LPS-mediated TNF-α in the arterial endothelial cells of rat kidneys [128]. In addition, in another animal experiment [129], genistein (10, 30, and 90 mg/kg injected i.p. 0.5 h before the LPS injection and 2 h and 8 h after the LPS injection) significantly improved the morphological structure, fiber protein deposition, function indicators (inhibition of blood urea nitrogen, BUN), and inflammation reaction (↓NF-κB, IL-6, and IL-1) in kidneys.…”

Section: The Effects Of Genistein On Common Kidney Diseasesmentioning

confidence: 99%

Effects of Genistein on Common Kidney Diseases

Peng

Shang

et al. 2022

Nutrients

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Genistein is a naturally occurring phytoestrogen (soy or soybean products) that is classified as an isoflavone, and its structure is similar to that of endogenous estrogens; therefore, genistein can exert an estrogen-like effect via estrogen receptors. Additionally, genistein is a tyrosine kinase inhibitor, which enables it to block abnormal cell growth and proliferation signals through the inhibition of tyrosine kinase. Genistein is also an angiogenesis inhibitor and an antioxidant. Genistein has effects on kidney cells, some of the kidney’s physiological functions, and a variety of kidney diseases. First, genistein exerts a protective effect on normal cells by reducing the inflammatory response, inhibiting apoptosis, inhibiting oxidative stress, inhibiting remodeling, etc., but after cell injury, the protective effect of genistein decreases or even has the opposite effect. Second, genistein can regulate renin intake to maintain blood pressure balance, regulate calcium uptake to regulate Ca2+ and Pi balances, and reduce vasodilation to promote diuresis. Third, genistein has beneficial effects on a variety of kidney diseases (including acute kidney disease, kidney cancer, and different chronic kidney diseases), such as reducing symptoms, delaying disease progression, and improving prognosis. Therefore, this paper reviews animal and human studies on the protective effects of genistein on the kidney in vivo and in vitro to provide a reference for clinical research in the future.

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Genistein has the function of alleviating and treating disseminated intravascular coagulation caused by lipopolysaccharide

Cited by 7 publications

References 73 publications

Ultramicronized Palmitoylethanolamide in the Management of Sepsis-Induced Coagulopathy and Disseminated Intravascular Coagulation

Ultramicronized Palmitoylethanolamide in the Management of Sepsis-Induced Coagulopathy and Disseminated Intravascular Coagulation

Salvianolic acid A alleviates lipopolysaccharide-induced disseminated intravascular coagulation by inhibiting complement activation

Effects of Genistein on Common Kidney Diseases

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