Puerarin Protects Against LPS-Induced Vascular Endothelial Cell Hyperpermeability via Preventing Downregulation of Endothelial Cadherin

Deng, Honghui; Wang, Sha; Wang, Xiaoli; Li, Lian; Fei, Xie; Zeng, Ziwei; Zhang, Wenxin

doi:10.1007/s10753-019-01014-0

Cited by 13 publications

(13 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It remains a great challenge to alleviate sepsis-induced endothelial injury. Moreover, recently some herbal medicines have been found to improve endothelial dysfunction and reduce inflammatory responses in LPS-induced HUVECs [8,9]. Therefore, more effective drugs are needed for protection against endothelial injury in sepsis.…”

Section: Introductionmentioning

confidence: 99%

Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy

You

Zhang

Geng

et al. 2021

BMC Complement Med Ther

View full text Add to dashboard Cite

Background Salidroside (SAL) is a bioactive compound extracted from Rhodiola rosea with various biological properties. This study was designed to explore the functions of SAL on the endothelial damage induced by lipopolysaccharide (LPS) and its related mechanisms. Methods Human umbilical vein endothelial cells (HUVECs) were pretreated with SAL (0, 10, 25, 50, 100 μM), and then incubated with LPS (10 μg/mL). Cell viability was evaluated by MTT assay, cell injury by lactate dehydrogenase (LDH) release, and inflammatory cytokines release by ELISA assay. Oxidative stress was evaluated by malondialdehyde (MDA) and superoxide dismutase (SOD) in cell lysate. Apoptosis was detected by flow cytometry and caspase-3 activity. Western blot were performed to determine expression levels of autophagy and NOD-like receptor protein 3 (NLRP3) related proteins. Results SAL at 50 μM concentration showed no toxicity on HUVECs, but attenuated LPS-induced injury, as evidenced by increased cell viability, reduction in LDH level and inflammatory cytokines in culture media. SAL also reduced MDA level and increased SOD activity in HUVECs, and inhibited apoptosis rate and caspase-3 activity. (P < 0.05). Moreover, LPS enhanced HUVECs autophagy, and SAL pretreatment further enhanced autophagy, with increased Beclin-1 protein and decreased P62 protein. SAL also attenuated LPS-induced activation of NLRP3 inflammasome, reduced the protein expression of NLRP3-related proteins, including ASC and caspase-1. Autophagy inhibition by 3-MA markedly reversed SAL-modulated changes in cell viability and NLRP3 expression in LPS-stimulated HUVECs. Conclusion SAL protects endothelial cells against LPS-induced injury through inhibition of NLRP3 pathways and enhancing autophagy.

show abstract

Section: Introductionmentioning

confidence: 99%

Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy

You

Zhang

Geng

et al. 2021

BMC Complement Med Ther

View full text Add to dashboard Cite

show abstract

“…However, all of the above-mentioned LPS-induced changes were improved by Puerarin pre-treatment. 36 Puerarin facilitated osteogenesis of steroid-induced necrosis of rabbit femoral head and osteogenesis of steroid-induced osteocytes via miR-34a upregulation. 37 In our study, Puerarin exhibited protective effects by reducing DNA damage and apoptosis of HUVECs caused by radiation.…”

Section: Discussionmentioning

confidence: 99%

Puerarin Reduces Radiation-Induced Vascular Endothelial Cell Damage Via miR-34a/Placental Growth Factor

Liu

Zhao

et al. 2022

Dose-Response

View full text Add to dashboard Cite

The aim is to explore the protective effects of Puerarin on radiation-induced vascular endothelial cell damage and its underlying mechanism. The apoptosis and DNA damage of Human umbilical vascular endothelial cells (HUVECs) exposed to radiation alone or in combination with glucose in the exposed group were significantly elevated ( P < .05) compared with those in the control group. The Puerarin-treated HUVECs showed significant reduction in the radiation-induced apoptosis and DNA damage ( P < .05). Furthermore, X-ray irradiation significantly increased the expression of miR-34a, which was reversed by pre-treatment with Puerarin. Placental Growth Factor (PLGF) was a target gene of miR-34a. The expression of PLGF in the peripheral blood of patients receiving radiotherapy significantly increased with an increase in the cumulative dose of radiation ( P < .05), after which it began to decrease at the fourth week ( P < .05) and then remained at a low level until the end of radiotherapy. Puerarin exerts a radioprotective effect by decreasing DNA damage and apoptosis through miR-34a-targeted PLGF.

show abstract

“…Samples of lung tissue were homogenized in radioimmunoprecipitation assay (RIPA) buffer supplemented with protease inhibitors, after which supernatant protein levels were quantified via BCA assay ( 12 ). Individual protein samples (30 μg) were then separated via 8-10% SDS-PAGE, and the resultant blots were probed with antibodies specific for aquaporin 5, VE-cadherin, claudin 18.1, NLRP3, HMGB1, TLR4, p-NF-κB, and β-actin (1:1000).…”

Section: Methodsmentioning

confidence: 99%

The protective role of raltegravir in experimental acute lung injury in vitro and in vivo

Ren

Jiang

2022

Braz J Med Biol Res

View full text Add to dashboard Cite

Disruption of pulmonary endothelial permeability and associated barrier integrity increase the severity of acute respiratory distress syndrome (ARDS). This study investigated the potential ability of the human immunodeficiency virus-1 (HIV-1) integrase inhibitor raltegravir to protect against acute lung injury (ALI) and the underlying mechanisms. Accordingly, the impact of raltegravir treatment on an in vitro lipopolysaccharide (LPS)-stimulated human pulmonary microvascular endothelial cell (HPMEC) model of ALI and an in vivo LPS-induced two-hit ALI rat model was examined. In the rat model system, raltegravir treatment alleviated ALI-associated histopathological changes, reduced microvascular permeability, decreased Evans blue dye extravasation, suppressed the expression of inflammatory proteins including HMGB1, TLR4, p-NF-kB, NLRP3, and MPO, and promoted the upregulation of protective proteins including claudin 18.1, VE-cadherin, and aquaporin 5 as measured via western blotting. Immunohistochemical staining further confirmed the ability of raltegravir treatment to reverse LPS-induced pulmonary changes in NLRP3, claudin 18.1, and aquaporin 5 expression. Furthermore, in vitro analyses of HPMECs reaffirmed the ability of raltegravir to attenuate LPS-induced declines in VE-cadherin and claudin 18.1 expression while simultaneously inhibiting NLRP3 activation and reducing the expression of HMGB1, TLR4, and NF-kB, thus decreasing overall vascular permeability. Overall, our findings suggested that raltegravir may represent a viable approach to treating experimental ALI that functions by maintaining pulmonary microvascular integrity.

show abstract

Puerarin Protects Against LPS-Induced Vascular Endothelial Cell Hyperpermeability via Preventing Downregulation of Endothelial Cadherin

Cited by 13 publications

References 18 publications

Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy

Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy

Puerarin Reduces Radiation-Induced Vascular Endothelial Cell Damage Via miR-34a/Placental Growth Factor

The protective role of raltegravir in experimental acute lung injury in vitro and in vivo

Contact Info

Product

Resources

About