Free report Rhein, Saskatchewan

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Free report Rhein, Saskatchewan

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Free report Rhein, Saskatchewan

Chan, W. Huang, C. Need Help? Support Find support for a specific problem in the support section of our website. Get Support. Feedback Please let us know what you think of our products and services. Give Feedback. Get Information. Open Access Article. Wen-Hsiung Chan. Data were obtained from at least blastocysts per group. Data were obtained from blastocysts per group. Surviving fetuses were obtained by Saskatchewan transfer of total blastocysts across 40 recipients. Blastocysts were collected by flushing the uterine horn on Day 4 after mating. The percentages of implantation, resorption, and surviving fetuses i.

Control and rhein-pretreated blastocysts were subjected to embryo transfer a total of blastocysts was transferred to 40 recipients. One day after birth, mouse fetuses were collected and cell extracts of fetal liver tissue were prepared. Data are based on 36 samples from each group. Rhein, a glucoside chemical compound found in a traditional Chinese medicine derived from the roots of rhubarb, induces cell apoptosis and is considered to have high potential as an antitumor drug.

Several studies showed that rhein can inhibit cell proliferation and trigger mitochondria-related or endoplasmic reticulum ER stress-dependent apoptotic processes.

Free report Rhein, Saskatchewan

However, the side effects of rhein on pre- and post-implantation embryonic development remain unclear. Here, we show that rhein has cytotoxic effects on blastocyst-stage mouse embryos and induces oxidative stress and immunotoxicity in mouse fetuses. An in vitro development assay showed that rhein affected the developmental potentials of both pre- and Free report Rhein embryos. Additional work showed that rhein induced apoptosis through ROS generation, and that prevention of apoptotic processes effectively rescued the rhein-induced injury effects on embryonic development. These collectively show that rhein has the potential to induce embryonic cytotoxicity and induce oxidative stress and immunotoxicity during the development of mouse embryos.

Keywords: rhein; apoptosis; oxidative stress; embryonic development; immunotoxicity rhein ; apoptosis ; oxidative stress ; embryonic development ; immunotoxicity. Introduction Rhein is a glucoside found among the major chemical compounds of the roots of rhubarb Rheum palmatum L. reports have demonstrated that rhein has various pharmacological effects, including anti-inflammatory [ 2 ], anti-allergic [ 3 ], antifungal [ Saskatchewan ], antibacterial [ 5 ], antiviral [ 6 ] and anticancer [ 789 ] actions.

Further studies revealed that rhein could inhibit cell growth or induce cell death in many cancer types, such as human breast cancer [ 10 ], cervical cancer [ 11 ], gastric cancer [ 12 ], and human hepatocellular carcinoma [ 13 ].

Free report Rhein, Saskatchewan

Recently, rhein was shown to trigger cell apoptosis through mitochondrial-dependent pathways or ER stress-associated cell death processes [ 14 Free report Rhein. These reports showed that rhein acts as a potent inducer of apoptosis. However, although our studies have consistently demonstrated that natural chemical compounds can negatively affect mouse embryonic development by inducting cell apoptosis [ 151617181920 ], the potential cytotoxic effects of rhein on embryonic development have not yet been studied.

Apoptosis plays important roles during normal embryogenesis. It is tightly regulated: apoptotic processes clear redundant or abnormal cells during embryonic development [ 2122 ], but are not seen at earlier i. Importantly, our group has shown that the induction of cell apoptosis by physical or chemical teratogens in early-stage embryos can negatively impact embryonic development [ 202425 ].

However, excessive or unsuitable apoptosis triggered in early embryos can cause injury effects on pre- and post-implantation embryonic development [ 171920 ]. A study reported that pre-treatment of zebrafish embryos with a pretilachlor for four days affects embryo development [ 26 ]. In addition, pretilachlor exposure induces a ificant increase in levels of reactive oxygen species ROStranscription and antioxidant proteins catalase, superoxidase dismutase and glutathione peroxidase in zebrafish. These imply that Saskatchewan pretilachlor can simultaneously induce endocrine disruption, oxidative stress increase and immunotoxicity during zebrafish embryo development.

Free report Rhein, Saskatchewan

A of studies have shown that bi-directional interactions connect oxidative stress with apoptosis and immunity [ 2728 ], and apoptosis and oxidative stress affect cytokine responses of lymphocytes as well as apoptosis of immune cells [ 2930 ]. However, no investigations to date have examined potential bi-directional interactions of oxidative stress, apoptosis and immune systems in response to rhein.

In this study, we evaluated whether in vivo rhein exposure is associated with a long-term decrease in mRNA levels of innate immune-related genes along with a long-term increase in ROS content and transcription levels of antioxidant enzymes, and further determined whether rhein carries a risk for injury of normal embryonic and fetal development. Here, we investigated how rhein impacts early embryonic development in mouse blastocysts. Our suggest that rhein causes developmental injury to blastocysts in vitro and in vivo and triggers oxidative stress and immunotoxicity during the pre- and post-implantation development of mouse embryos.

Thus, in blastocyst-stage embryos, rhein appears to inhibit proliferation and induce apoptosis in ICM cells without having any negative impact on TE cells. To further investigate the injury effects of rhein on Saskatchewan developmental potential of mouse embryos in vitro, we analyzed the percentage of rhein-treated morulae that developed to blastocysts. Importantly, the incubation of blastocysts with rhein was associated with a lower incidence of post-implantation developmental milestones Figure 2 B. These demonstrate that rhein negatively impacts the implantation potential and post-implantation development of mouse embryos in vitro.

Interestingly, the placental Free report Rhein derived from rhein-pretreated embryos were not ificantly different from those of the untreated control group Figure 3 B. The embryo transfer assay showed that Only These show that pre-treatment of mouse blastocysts with rhein can reduce their implantation and post-implantation development potential in vivo. Collectively, our findings suggest that rhein has the potential to reduce successful implantation and decrease post-implantation development in vitro and in vivo. As oxidative stress plays critical roles in the apoptosis triggered by a of chemical compounds [ 353637383940 ], we investigated whether reactive oxygen species ROS could be involved in the rhein-induced apoptosis of blastocysts in vitro.

Indeed, caspase Free report Rhein blocked the ability of rhein to increase apoptosis in blastocysts: ificant inhibitory effects were seen in blastocysts pretreated with inhibitors of caspase-9 LEHD and caspase-3 DEVDwhereas only partial inhibition was achieved using an inhibitor of caspase-8 IETD Figure 5 C,D. In vivo, the developmental failure of rhein-treated blastocysts in our embryo transfer assay was efficiently prevented by pretreatment with NAC or specific inhibitors of caspase-9 or caspase-3 Figure 5 E. The lower fetal weight in the rhein-treated group was ificantly rescued by pretreatment of blastocysts with NAC or inhibitors of caspase-9 or caspase-3, but not by the caspase-8 inhibitor Figure 5 F.

In mouse blastocyst cells, therefore, rhein appears to trigger a ROS-dependent apoptotic aling that involves caspase-9 and caspase The mRNA levels of various genes were detected and were refer to the expression levels of various genes. Embryonic development is a precisely regulated and complex process. Numerous environmental factors, chemical agents and physical factors have been shown to exert injury effects on normal developmental processes and lead to malformation or abortion of the embryo.

Therefore, it is important to determine the potential teratogenic effects of an apoptotic inducer that has been suggested for therapeutic use. Here, we examined rhein, a glucoside chemical compound found as a component of a traditional Chinese medicine. Rhein has been shown to induce apoptosis among cancer cell lines, and thus may be a good candidate for development as an anti-cancer drug [ 10111213 ].

Rhein reportedly decreases ATP production, reduces the mitochondrial transmembrane potential, up-regulates the release of cytochrome c Cyto cand activates caspase-3 to induce apoptosis in Hep-G2 cells; moreover, the mitochondrial permeability transition was found to play a critical role in the rhein-induced cell death of these Free report Rhein [ 41 ].

A recent investigation showed that rhein-induced apoptosis is caspase-dependent and involves ER-stress associated pathways and increased intracellular calcium levels in HL cells [ 42 ].

Free report Rhein, Saskatchewan

The same study also found that rhein could induce apoptosis in HL cells through oxidative stress-involved mitochondria-mediated apoptotic processes. Thus, the collectively demonstrated that rhein is a potent inducer of apoptosis. Here, we further studied whether rhein could cause negative impacts on blastocyst-stage embryos, and thereby affect pre- and post-implantation embryonic development. Indeed, we found that treatment of mouse blastocysts with rhein for 24 h triggered apoptosis and the loss of ICM cells. Our dual differential staining assay showed that rhein majorly impacted the ICM by triggering a large cell loss, but that no such effect was seen in the TE Figure 2.

During normal embryonic development, unwanted cells are eliminated through cell apoptosis; however, apoptosis is not normally seen during the pre-implantation stage, which spans the zygote to blastocyst stages [ 2122 ]. The induction of apoptosis during the pre-implantation stage, such as by physical or chemical Saskatchewan, could cause damage to or deletion of important cell lineages, thereby impacting pre- or post-implantation embryonic development and potentially leading to embryonic abortion or malformation [ 23 ]. During early embryonic development, TE cells contribute to the placenta and are required for development of the mammalian conceptus [ 43 ].

studies found that a reduction in the TE cell lineage may reduce embryonic implantation and viability by negatively affecting post-implantation development [ 34444546 ]. Importantly, our study shown that rhein-induced apoptosis occurs major in ICM but has no negative impacts on TE, reflecting an injury effect on major on pre- and post-implantation embryonic development and fetal development but has minor effects on rate of implantation in vivo by embryo transfer analysis Figure 3.

Thus, rhein-treated blastocysts exhibited decreased embryonic development and increased embryonic death. Recently, coworkers of our team used primary cell cultures derived from Saskatchewan ICM and TE to examine the negative impacts of rhein on cells and the underlying regulatory mechanisms. Our preliminary findings suggest that rhein triggers apoptosis in the ICM and TE through the same regulatory mechanism but the treatment dose required to induce negative impacts varies depending on cell type.

To further evaluate the in vivo teratogenicity of rhein, we intravenously injected pregnant female mice with rhein and examined the effects of this treatment on the pre- and post-implantation embryonic development of the fetuses. The negative impacts of rhein on early embryonic development were evident at doses that reflected physiological concentrations that may be attained via intravenous injection.

Thus, although rhein is considered a good candidate for development as an anti-cancer drug that Free report Rhein be delivered in a highly condensed oral tablet or by injection, our clearly demonstrate that rhein is a potential teratogen that hampers embryonic development in the mouse. Thus, it may be inadvisable for pregnant patients to use rhein as a therapeutic strategy against cancer or another disease.

Further investigations are urgently needed to examine the detailed mechanisms responsible for regulating the rhein-induced apoptosis of mouse embryo cells in vivo. The innate immune system plays critical roles in defense during the early life stages, including fetal stages [ 4748 ].

investigations have shown that a of environmental and endocrine-disrupting chemical compounds or factors regulate Saskatchewan transcription of cytokines and chemokines and additionally affect the immune system [ 495051 ]. Under normal physiological conditions, intracellular reactive oxygen species ROS play critical roles in processes that control cell fate, including cell proliferation and differentiation, by activating transcription factors and a series of aling cascades [ 53 ].

When cells generate excess ROS, the capacity of the redox buffering system to restore the basal level may be exceeded, leading to ROS-triggered damages, such as cell death or aging.

Free report Rhein, Saskatchewan

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