Lycium�barbarum polysaccharides protect human trophoblast HTR8/SVneo cells from hydrogen peroxide‑induced oxidative stress and apoptosis

Li, Jing; Ding, Zhongjun; Yang, Yanwen; Mao, Baohong; Wang, Yanxia; Xu, Xiaoying

doi:10.3892/mmr.2018.9274

Cited by 12 publications

(12 citation statements)

References 56 publications

(42 reference statements)

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“…It is well established that H2O2 could be used to stimulate oxidative stress in vitro [30][31][32]. In the present study, we found that treatment with 400 μM H2O2 resulted in decreased cell viability in HTR8/SVneo cells, which is consistent with a previous study [1]. Curcumin has been reported to be toxic at a high dose, while it exerts a strong antioxidant effect at a low dose [23].…”

Section: Discussionsupporting

confidence: 92%

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Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

Jiang

Zhang

et al. 2020

Antioxidants

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Pregnancy complications are associated with oxidative stress induced by accumulation of trophoblastic ROS in the placenta. We employed the human trophoblast HTR8/SVneo cell line to determine the effect of curcumin pre-treatment on H2O2-induced oxidative damage in HTR8/Sveo cells. Cells were pretreated with 2.5 or 5 μM curcumin for 24 h, and then incubated with 400 μM H2O2 for another 24 h. The results showed that H2O2 decreased the cell viability and induced excessive accumulation of reactive oxygen species (ROS) in HTR8/Sveo cells. Curcumin pre-treatment effectively protected HTR8/SVneo cells against oxidative stress-induced apoptosis via increasing Bcl-2/Bax ratio and decreasing the protein expression level of cleaved-caspase 3. Moreover, curcumin pre-treatment alleviated the excessive oxidative stress by enhancing the activity of antioxidative enzymes. The antioxidant effect of curcumin was achieved by activating Nrf2 and its downstream antioxidant proteins. In addition, knockdown of Nrf2 by Nrf2-siRNA transfection abolished the protective effects of curcumin on HTR8/SVneo cells against oxidative damage. Taken together, our results show that curcumin could protect HTR8/SVneo cells from H2O2-induced oxidative stress by activating Nrf2 signaling pathway.

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Section: Discussionsupporting

confidence: 92%

“…Intrauterine growth retardation (IUGR) and preeclampsia (PE) are detrimental pregnancy complications that could cause significant increased perinatal morbidity and mortality [1]. Normal placental development during early pregnancy depends entirely on the differentiation, proliferation, and invasion of trophoblast cells [2].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

Jiang

Zhang

et al. 2020

Antioxidants

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“…The peroxidative environment was simulated in our experiments by using hydrogen peroxide at similar concentrations as those previously used in the same cell lines [37,60], since it is physiologically produced in maternal circulation and its levels are increased in preeclamptic patients in the early stages of pregnancy [61]. Also, the concentration of hydrogen peroxide was similar to the one that has been shown to cause senescence in hUSMCs [60].…”

Section: Discussionmentioning

confidence: 99%

“…The used concentrations of hCG and estradiol were in the range of plasma values found in humans [35,36]. Also hydrogen peroxide was used at a concentration similar to the one previously used in the same cell lines [37]. The culture medium from hUMSCs was also collected and used for co-stimulation experiments after centrifugation and filtration.…”

Section: Methodsmentioning

confidence: 99%

Preeclampsia and intrauterine growth restriction: Role of human umbilical cord mesenchymal stem cells-trophoblast cross-talk

et al. 2019

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Background Oxidative stress is involved in the pathogenesis and maintenance of pregnancy-related disorders, such as intrauterine growth restriction (IUGR) and preeclampsia (PE). Human umbilical cord mesenchymal stem cells (hUMSCs) have been suggested as a possible therapeutic tool for the treatment of pregnancy-related disorders in view of their paracrine actions on trophoblast cells. Objectives To quantify the plasma markers of peroxidation in patients affected by PE and IUGR and to examine the role of oxidative stress in the pathophysiology of PE and IUGR in vitro by using hUMSCs from physiological and pathological pregnancies and a trophoblast cell line (HTR-8/SVneo). Study design In pathological and physiological pregnancies the plasma markers of oxidative stress, arterial blood pressure, serum uric acid, 24h proteinuria, weight gain and body mass index (BMI) were examined. Furthermore, the pulsatility index (PI) of uterine and umbilical arteries, and of fetal middle cerebral artery was measured. In vitro , the different responses of hUMSCs, taken from physiological and pathological pregnancies, and of HTR-8/SVneo to pregnancy-related hormones in terms of viability and nitric oxide (NO) release were investigated. In some experiments, the above measurements were performed on co-cultures between HTR-8/SVneo and hUMSCs. Results The results obtained have shown that in pathological pregnancies, body mass index, serum acid uric, pulsatility index in uterine and umbilical arteries and markers of oxidative stress were higher than those found in physiological ones. Moreover, in PE and IUGR, a relation was observed between laboratory and clinical findings and the increased levels of oxidative stress. HTR-8/SVneo and hUMSCs showed reduced viability and increased NO production when stressed with H 2 O 2 . Finally, HTR-8/SVneo cultured in cross-talk with hUMSCs from pathological pregnancies showed a deterioration of cell viability and NO release when treated with pregnancy-related hormones. Conclusion Our findings support that hUMSCs taken from patients affected by PE and IUGR have significant features in comparison with those from physiologic pregnancies. Moreover, the cross-talk between hUMSCs and trophoblast cells might be involved in the etiopathology of IUGR and PE secondary to oxidative stress.

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“…Since sPIF modulated inflammation during pregnancy (Fig 1) [20], we decided to test sPIF in challenged placental cells next. We chose to test pro-inflammatory (IL-6 and NLRP4) and proapoptotic (Bad and Bax) genes as they contribute to pregnancy complications such as PTB [5,20,51,52]. We detected moderate changes after sPIF-only treatment (Fig 2A and 2B; compare green to black bars).…”

Section: Synthetic Pif Reduces the Inflammatory Response (In-vivo)mentioning

confidence: 99%

Synthetic PreImplantation Factor (sPIF) reduces inflammation and prevents preterm birth

et al. 2020

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Preterm birth (PTB) is the leading cause of neonatal morbidity and mortality and spontaneous PTB is a major contributor. The preceding inflammation/infection contributes not only to spontaneous PTB but is associated with neonatal morbidities including impaired brain development. Therefore, control of exaggerated immune response during pregnancy is an attractive strategy. A potential candidate is synthetic PreImplantation Factor (sPIF) as sPIF prevents inflammatory induced fetal loss and has neuroprotective properties. Here, we tested maternal sPIF prophylaxis in pregnant mice subjected to a lipopolysaccharides (LPS) insult, which results in PTB. Additionally, we evaluated sPIF effects in placental and microglial cell lines. Maternal sPIF application reduced the LPS induced PTB rate significantly. Consequently, sPIF reduced microglial activation (Iba-1 positive cells) and preserved neuronal migration (Cux-2 positive cells) in fetal brains. In fetal brain lysates sPIF decreased IL-6 and INFγ concentrations. In-vitro, sPIF reduced Iba1 and TNFα expression in microglial cells and reduced the expression of pro-apoptotic (Bad and Bax) and inflammatory (IL-6 and NLRP4) genes in placental cell lines. Together, maternal sPIF prophylaxis prevents PTB in part by controlling exaggerated immune response. Given the sPIF'FDA Fast Track approval in non-pregnant subjects, we envision sPIF therapy in pregnancy.

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Lycium�barbarum polysaccharides protect human trophoblast HTR8/SVneo cells from hydrogen peroxide‑induced oxidative stress and apoptosis

Cited by 12 publications

References 56 publications

Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway

Preeclampsia and intrauterine growth restriction: Role of human umbilical cord mesenchymal stem cells-trophoblast cross-talk

Synthetic PreImplantation Factor (sPIF) reduces inflammation and prevents preterm birth

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