Ginkgolide B induces apoptosis and developmental injury in mouse embryonic stem cells and blastocysts

Abstract

Our results reveal for the first time that ginkgolide B retards the proliferation and development of mouse ESCs and blastocysts in vitro and causes developmental injury in vivo.

Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

“…Analysis of EB formation and MAP-2 expression in embryonic stem cells during NGF-induced cell differentiation confirmed that CTN caused early embryonic developmental injury (Figures 7A and 7B). Our previous studies demonstrated that apoptotic injury due to chemical treatment had significant negative effects on embryonic development [10,46]. In the present study, I have shown that CTN-induced apoptosis led to a high injury risk during early embryonic development.…”

“…EBs were generated as previously described [10]. Briefly, ESC-B5 cells were dissociated with trypsin-EDTA (0.25 %) and cultured in LIF (leukaemia inhibitory factor)-free stem cell medium to induce differentiation.…”

“…In view of the previous finding that ROS effectively induces stem cell apoptosis [10], I next used the fluorescent dyes, DCFH-DA and rhodamine 123, to examine whether the ROS content increased in CTN-treated ESC-B5 cells. As shown in Figure 3(A), 10-30 µM CTN directly induced a ∼ 7-18-fold increase in the intracellular ROS content of ESC-B5 cells, compared with untreated control cells.…”

“…However, apoptotic processes do not occur prior to the blastocyst stage during normal mouse embryonic development [8], and induction of apoptosis during the early stages of embryogenesis (i.e. by exposure to a teratogen) has been shown to cause embryonic developmental injury [9,10]. Many of the chemical and physical treatments that induce apoptosis stimulate oxidative stress via generation of ROS (reactive oxygen species) [9,[11][12][13], suggesting a close relationship between oxidative stress and apoptosis.…”

Quercetin Improves In Vitro Development of Porcine Oocytes by Decreasing Reactive Oxygen Species Levels.

“…We suggest that the reduction of oocyte maturation and blastocyst formation rates with this concentration of quercetin may result from unresponsive signaling to oocytes and embryos or direct embryo toxicity owing to excessive levels of flavonoids. Some groups have reported toxic effects of other flavonoids on embryos from different species [4][5][6]27]. In contrast, several investigations have shown that supplementation of porcine IVM medium with antioxidants such as selenium, vitamin E, and ascorbic acid decreases ROS levels while enhancing the developmental competence of IVF embryos and parthenotes [21,29,30].…”