Artemisinin protects endothelial function and vasodilation from oxidative damage via activation of PI3K/Akt/eNOS pathway

Wang, Peng; Tian, Xiaoying; Tang, Juxian; Xiao, Duan; Wang, Jinying; Chen, Huan; Qiu, Xiaoyuan; Wang, Wenxuan; Mai, Mengfei; Yang, Qinghua; Liao, Rifang; Yan, F.

doi:10.1016/j.exger.2021.111270

Cited by 14 publications

(9 citation statements)

References 38 publications

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“…In contrast, inhibition of the PI3K/Akt pathway is associated with reducing eNOS phosphorylation and inhibits NO production, which is associated with endothelial cell dysfunction [ 57 ]. Previous studies have reported that artemisinin can suppresscell death induced by hydrogen peroxicde and protect HUVECs function from oxidative damage through activation of the PI3K/Akt/eNOS pathway [ 58 ]. In this research, we show that PGZ-Exos promote the expression of p-AKT, p-PI3K and p-eNOS, which in turn promote angiogenesis through the PI3K/AKT/eNOS pathway.…”

Section: Discussionmentioning

confidence: 99%

Exosomes derived from pioglitazone-pretreated MSCs accelerate diabetic wound healing through enhancing angiogenesis

et al. 2021

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Background Enhanced angiogenesis can promote diabetic wound healing. Mesenchymal stem cells (MSCs)-derived exosomes, which are cell-free therapeutics, are promising candidates for the treatment of diabetic wound healing. The present study aimed to investigate the effect of exosomes derived from MSCs pretreated with pioglitazone (PGZ-Exos) on diabetic wound healing. Results We isolated PGZ-Exos from the supernatants of pioglitazone-treated BMSCs and found that PGZ-Exos significantly promote the cell viability and proliferation of Human Umbilical Vein Vascular Endothelial Cells (HUVECs) injured by high glucose (HG). PGZ-Exos enhanced the biological functions of HUVECs, including migration, tube formation, wound repair and VEGF expression in vitro. In addition, PGZ-Exos promoted the protein expression of p-AKT, p-PI3K and p-eNOS and suppressed that of PTEN. LY294002 inhibited the biological function of HUVECs through inhibition of the PI3K/AKT/eNOS pathway. In vivo modeling in diabetic rat wounds showed that pioglitazone pretreatment enhanced the therapeutic efficacy of MSCs-derived exosomes and accelerated diabetic wound healing via enhanced angiogenesis. In addition, PGZ-Exos promoted collagen deposition, ECM remodeling and VEGF and CD31 expression, indicating adequate angiogenesis in diabetic wound healing. Conclusions PGZ-Exos accelerated diabetic wound healing by promoting the angiogenic function of HUVECs through activation of the PI3K/AKT/eNOS pathway. This offers a promising novel cell-free therapy for treating diabetic wound healing. Graphic abstract

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Section: Discussionmentioning

confidence: 99%

Exosomes derived from pioglitazone-pretreated MSCs accelerate diabetic wound healing through enhancing angiogenesis

et al. 2021

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“…16 Moreover, Wang et al exposed that artemisinin could curb oxidative injury of human umbilical vein endothelial cells through activating the PI3K/Akt/endothelial nitric oxide synthase pathway. 17 In this research, we will analyze the role of PI3K/Akt signaling in cerebral hemorrhage.…”

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confidence: 99%

Kurarinone alleviates hemin‐induced neuroinflammation and microglia‐mediated neurotoxicity by shifting microglial M1/M2 polarization via regulating the IGF1/PI3K/Akt signaling

Jia

Zuo

Yue

2022

The Kaohsiung J of Med Scie

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Cerebral hemorrhage is a fatal disease that causes severe damage to local nerve function. The purpose of this research is to analyze the effect of kurarinone on hemin‐induced neuroinflammation and neurotoxicity. In our study, according to the results of bioinformatics analysis, we hypothesized that kurarinone might modulate cerebral hemorrhage advancement via the insulin‐like growth factor 1/phosphoinositide 3‐kinase/protein kinase B (IGF1/PI3K/Akt) signaling. Kurarinone promoted M2 microglia polarization, and curbed M1 polarization and inflammation in human microglial cells (HMC3) cells with hemin treatment. Besides, kurarinone upregulated IGF1 expression and activated the PI3K/Akt signaling pathway in hemin‐treated HMC3 cells. In addition, downregulation of IGF1 or inhibition of the PI3K/Akt signaling weakened the effects of kurarinone on microglia polarization and inflammation in HMC3 cells with hemin treatment. Kurarinone alleviated apoptosis and oxidative damage of SH‐SY5Y cells co‐cultured with hemin‐treated HMC3 cells. In conclusion, kurarinone lessened hemin‐induced neuroinflammation and microglia‐mediated neurotoxicity by regulating microglial polarization through modulating the IGF1/PI3K/Akt signaling. These results delivered a new prospective therapeutic drug for the treatment of cerebral hemorrhage.

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“…PI3K/AKT signaling is an important pathway involved in the modulation of redox balance. Activation of PI3K/AKT enhances the antioxidant effect ( Kim et al, 2021 ; Wang P et al, 2021 ). The PI3K/AKT signaling pathway has been demonstrated to have a positive effect on osteoblast differentiation and inhibition of PI3K/AKT signaling suppresses the osteoinduction process ( Zhang et al, 2019 ; Dong et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Metformin Promotes Differentiation and Attenuates H2O2-Induced Oxidative Damage of Osteoblasts via the PI3K/AKT/Nrf2/HO-1 Pathway

et al. 2022

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At present, the drug treatment of osteoporosis is mostly focused on inhibiting osteoclastogenesis, which has relatively poor effects. Metformin is a drug that can potentially promote osteogenic differentiation and improve bone mass in postmenopausal women. We aimed to detect the molecular mechanism underlying the osteogenic effect of metformin. Our study indicated that metformin obviously increased the Alkaline phosphatase activity and expression of osteogenic marker genes at the mRNA and protein levels. The PI3K/AKT signaling pathway was revealed to play an essential role in the metformin-induced osteogenic process, as shown by RNA sequencing. We added LY294002 to inhibit the PI3K/AKT pathway, and the results indicated that the osteogenic effect of metformin was also blocked. Additionally, the sequencing data also indicated oxidation-reduction reaction was involved in the osteogenic process of osteoblasts. We used H2O2 to mimic the oxidative damage of osteoblasts, but metformin could attenuate it. Antioxidative Nrf2/HO-1 pathway, regarded as the downstream of PI3K/AKT pathway, was modulated by metformin in the protective process. We also revealed that metformin could improve bone mass and oxidative level of OVX mice. In conclusion, our study revealed that metformin promoted osteogenic differentiation and H2O2-induced oxidative damage of osteoblasts via the PI3K/AKT/Nrf2/HO-1 pathway.

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Artemisinin protects endothelial function and vasodilation from oxidative damage via activation of PI3K/Akt/eNOS pathway

Cited by 14 publications

References 38 publications

Exosomes derived from pioglitazone-pretreated MSCs accelerate diabetic wound healing through enhancing angiogenesis

Exosomes derived from pioglitazone-pretreated MSCs accelerate diabetic wound healing through enhancing angiogenesis

Kurarinone alleviates hemin‐induced neuroinflammation and microglia‐mediated neurotoxicity by shifting microglial M1/M2 polarization via regulating the IGF1/PI3K/Akt signaling

Metformin Promotes Differentiation and Attenuates H2O2-Induced Oxidative Damage of Osteoblasts via the PI3K/AKT/Nrf2/HO-1 Pathway

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