scholarly journals Effects and Mechanism of Oxymatrine Combined with Compound Yinchen Granules on the Apoptosis of Hepatocytes through the Akt/FoxO3a/Bim Pathway

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Xian Zhang ◽  
Jiajia Ge ◽  
Xuejuan Zhu ◽  
Haifeng Zhang ◽  
Yuanzi Wang ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Western Blot ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Rat Liver ◽  
Caspase 3 ◽  
Normal Group ◽  
Model Group ◽  
Apoptosis Rate ◽  
Liver Tissues

The aim of the present study was to investigate the effects and mechanism of oxymatrine (OMT) combined with compound yinchen granules (CYG) on the apoptosis of hepatocytes through the Akt/FoxO3a/Bim pathway in rats with acute liver failure. The rat model of acute liver failure was established using lipopolysaccharide/D-galactosamine (LPS/D-GalN). The expression of proteins in rat liver tissues was detected by western blot analysis. The mRNA expression of FoxO3a, Bim, Bax, Bcl-2, and caspase-3 in rat liver tissues was detected by RT-qPCR. The apoptosis rate of rat hepatocytes was determined by flow cytometry. Western blots showed that when compared with the normal group, the expression of p-Akt and p-FoxO3a in the model group was decreased ( P < 0.05 ), while the expression of Bim was increased ( P < 0.01 ). Compared with the model group, the expression of p-Akt and p-FoxO3a in the OMT group and the OMT combined with CYG groups was increased ( P < 0.05 or P < 0.01 ), while the expression of Bim was decreased ( P < 0.05 ). The Bax/Bcl-2 ratio and caspase-3 protein expression in the model group were significantly higher than those in the normal group ( P < 0.01 ). The Bax/Bcl-2 ratio and the expression of caspase-3 protein in the OMT group and the OMT combined with CYG groups were significantly lower than those in the model group ( P < 0.01 ). The results of RT-qPCR were consistent with those of western blot. The results of flow cytometry showed that the apoptosis rate of hepatocytes in the OMT group and the OMT combined with CYG groups was significantly lower than that in the model group ( P < 0.05 or P < 0.01 ). We concluded that LPS/D-GalN can induce apoptosis of hepatocytes in rats with acute liver failure through the Akt/FoxO3a/Bim pathway. OMT combined with CYG inhibits apoptosis of hepatocytes in rats with acute liver failure via the Akt/FoxO3a/Bim pathway.

scholarly journals Ovarian Cancer HO-8910 Cell Apoptosis Induced by Crocin in vitro

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Dan Xia
Keyword(s):  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Western Blot ◽  
Blot Analysis ◽  
Cell Apoptosis ◽  
Western Blot Analysis ◽  
Caspase 3 ◽  
Cell Cycle Distribution ◽  
Apoptotic Pathway ◽  
Apoptosis Rate

The effect and mechanism of ovarian cancer HO-8910 cell apoptosis induced by crocin. MTT assay was performed to detect the inhibitory action of crocin on the proliferation of HO-8910 cells. Flow cytometry was used to test the cell cycle distribution and apoptosis rate of ovarian cancer HO-8910 cells. Western blot analysis was utilized to measure the levels of apoptotic proteins such as p53, Fas/APO-1, and Caspase-3. MTT analysis revealed that crocin significantly inhibited the growth of HO-8910 cells. Additionally, flow cytometry illustrated that crocin raised the proportion of HO-8910 cells in the G0/G1 phase and increased their apoptosis rate. Furthermore, Western blot analysis revealed that crocin up-regulated the expression of p53, Fas/APO-1, and Caspase-3. The results of this study showed that crocin can significantly inhibit the growth of HO-8910 cells and arrest them in the G0/G1 phase. Crocin can also promote ovarian cancer HO-8910 cell apoptosis, most likely by increasing p53 and Fas/APO-1 expression, and then activating the apoptotic pathway regulated by Caspase-3.

scholarly journals An Immunomodulatory Protein (Ling Zhi-8) from aGanoderma lucidumInduced Acceleration of Wound Healing in Rat Liver Tissues after Monopolar Electrosurgery

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Hao-Jan Lin ◽  
Yushan-Sophie Chang ◽  
Li-Hsiang Lin ◽  
Chiung-Fang Haung ◽  
Chia-Yu Wu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Western Blot ◽  
Rat Liver ◽  
Blot Analysis ◽  
Liver Tissue ◽  
Caspase 3 ◽  
Dapi Staining ◽  
Monopolar Electrosurgery ◽  
Immunomodulatory Protein ◽  
Liver Tissues

The purpose of this study was to investigate the effect of an immunomodulatory protein (Ling Zhi-8, LZ-8) on wound healing in rat liver tissues after monopolar electrosurgery. Animals were sacrificed for evaluations at 0, 3, 7, and 28 days postoperatively. It was found that the wound with the LZ-8 treatment significantly increases wound healing. Western blot analysis clearly indicated that the expression of NF-κB was decreased at 3, 7, and 28 days when liver tissues were treated with LZ-8. Moreover, caspase-3 activity of the liver tissue also significantly decreases at 7 and 28 days, respectively. DAPI staining and TUNEL assays revealed that only a minimal dispersion of NF-κB was found on the liver tissue treated with LZ-8 at day 7 as compared with day 3 and tissues without LZ-8 treatment. Similarly, apoptosis was decreased on liver tissues treated with LZ-8 at 7 days when compared to the control (monopolar electrosurgery) tissues. Therefore, the analytical results demonstrated that LZ-8 induced acceleration of wound healing in rat liver tissues after monopolar electrosurgery.

scholarly journals Betaine ameliorates intestinal injury by targeting the LPS/TLR4/MyD88 pathway and microbial communities of intestinal tract in acute liver failure

2019 ◽  
Author(s):  
Qian Chen ◽  
Yao Wang ◽  
Fang-Zhou Jiao ◽  
Chun-Xia Shi ◽  
Mao-Hua Pei ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Relative Abundance ◽  
Normal Group ◽  
Mucosal Barrier ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Model Group ◽  
Intestinal Epithelial Barrier ◽  
Gut Microbiota Composition

Abstract Background: A growing body of evidence revealed that the gut microbiome has a marked impact in acute liver failure (ALF). Microbes and their products will translocate into enterocoelia and enter into circulation system from the damaged intestinal lumen. It will further aggravate liver injury by enhancing the spread of inflammation, tissue damage and sepsis. Betaine is a hepatoprotective drug which has anti-inflammatory and anti-oxidant effects. Here, we evaluated the impact of betaine on gut microbiota composition in ALF animal experiment. The potential protective effect of betaine by inhibiting Toll-like receptor 4 (TLR4) responses was explored as well.Results: Eighteen mice were randomly divided into normal, model, and betaine groups. The ALF-induced intestinal epithelial barrier disruption internal models were induced by D-galactosamine（D-Gal）and lpopolysaccharide (LPS). Betaine was administered intragastrically 1 week before exposure of D-Gal/LPS. LPS were solely applied with a rat small intestinal cell line IEC-18 to establish ALF-induced intestinal epithelial barrier disruption external model. Mice in the model group developed severe intestinal epithelial tissue injury than normal group, increased significantly in the protein levels of TLR4, MyD88, TRAF6 and TNF-a and the mRNA levels of TLR4 and MyD88, and decreased significantly in the protein and mRNA levels of (ZO)-1 and occludin. Whereas, all above indicators were improved significantly by administration of betaine than that in model. The degree of liver tissue pathological damage, liver function and serum inflammatory cytokines in betaine group were significantly reduced than that in model group. The permeability of mice intestinal epithelial and IEC-18 cell in models was improved in betaine group than models. A total of 509 Operational Taxonomic Units (OTUs) were produced from mice fecal samples according to 16s rRNA gene sequence analysis. There were 156 core microbiomes in fecal samples. There existed a total of 24 species contained 11 species at the genus level which had a significant difference between groups. The increased relative abundance of g-Enterorhabdus in the model group was detected compared with normal group. Betaine down-regulated the relative abundance of g-Enterorhabdus in model. The relative abundance of g-Bacteroides was the highest in normal group and the least in model group. The relative abundance of g-Prevotella was almost identical in normal and betaine group, and it was decreased in model group.Conclusion: Betaine effectively improved the intestinal mucosal barrier in acute liver failure. The mechanism was probably related to inhibit the LPS/TLR4/MyD88 signaling pathways, improved the intestinal mucosal barrier and then maintained the gut microbiota composition.

scholarly journals The Protective Mechanism of CAY10683 on Intestinal Mucosal Barrier in Acute Liver Failure through LPS/TLR4/MyD88 Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Yao Wang ◽  
Hui Chen ◽  
Qian Chen ◽  
Fang-Zhou Jiao ◽  
Wen-Bin Zhang ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Mucosal Barrier ◽  
Protective Mechanism ◽  
Epithelial Tissue ◽  
Intestinal Epithelial ◽  
Model Group ◽  
Intestinal Mucosal Barrier ◽  
Protein Levels ◽  
Myd88 Pathway

The purpose of this study was to investigate the protective mechanism of HDAC2 inhibitor CAY10683 on intestinal mucosal barrier in acute liver failure (ALF). In order to establish ALF-induced intestinal epithelial barrier disruption models, D-galactosamine/LPS and LPS were, respectively, used with rats and NCM460 cell and then administrated with CAY10683. Transepithelial electrical resistance (TEER) was measured to detect the permeability of cells. Real-time PCR and Western blotting were employed to detect the key mRNA and protein levels. The intestinal epithelial tissue pathology was detected. After interfering with CAY10683, the mRNA and protein levels of TLR4, MyD88, TRIF, and TRAF6 were decreased compared with model group (P<0.05), whereas the levels of ZO-1 and occluding were elevated (P<0.05). The permeability was elevated in CAY10683-interfered groups, when compared with model group (P<0.05). And the degree of intestinal epithelial tissue pathological damage in CAY10683 group was significantly reduced. Moreover, CAY10683 significantly decreased the TLR4 staining in animal tissue. The HDAC2 inhibitor CAY10683 could promote the damage of intestinal mucosal barrier in ALF through inhibiting LPS/TLR4/MyD88 pathway.

Effects of riluzole (RZ) and ionizing radiation (IR) in metabotropic glutamate receptor-1 (GRM1) positive human melanoma

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 9083-9083
Author(s):  
C. Green ◽  
D. Schiff ◽  
A. Khan ◽  
S. Goyal ◽  
J. Goydos ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Western Blot ◽  
Cell Survival ◽  
Glutamate Receptor ◽  
Blot Analysis ◽  
Caspase 3 ◽  
Metabotropic Glutamate Receptor ◽  
Human Melanoma ◽  
Metabotropic Glutamate

9083 Background: Melanoma has long been known to be relatively radio-resistant. GRM1 is a metabotropic glutamate receptor that has been detected in human melanoma cell lines and biopsies. Riluzole (RZ), a glutamate release inhibitor, has been shown to arrest GRM1 positive human melanoma cells in G2/M and sub-G1 phases of the cell cycle. The purpose of this study was to determine if RZ enhances the lethal effects of IR in human melanoma. Methods: ATP luminescence assays were performed. Clonogenic assays were performed and cell survival curves generated. Cell cycle analysis was performed utilizing flow cytometry. Western blot analysis was performed utilizing cleaved PARP and caspase-3 antibodies as markers of apoptosis. Results: Luminescence assays revealed 25uM Riluzole to be the necessary concentration for clonogenic assays. At 2Gy, there was a 48% reduction (p≤0.05) in cell survival in RZ-treated cells. At 4 Gy, there was a 19% reduction (p≤0.05) in cell survival in RZ-treated cells. No differences were seen at 6 and 8 Gy. Cell cycle analysis showed that the combination of IR and RZ was superior to IR alone in increasing the number of cells in sub-G1, which represents apoptotic death. Western blot analysis showed that the combination of IR and RZ showed yielded increased cleaved PARP and caspase-3 activity when compared to IR alone. Conclusions: Riluzole is a FDA approved drug that has long been used in ALS. It is relatively non-toxic and crosses the blood brain barrier. Our data shows that Riluzole in combination with radiation eliminates the radio-resistant shoulder of the C8161 survival curve. RZ and IR, as combination therapy are more lethal than IR or RZ alone in human melanoma, as demonstrated by flow cytometry and WB analysis. This data has promising implications for melanoma patients with brain metastases. No significant financial relationships to disclose.

scholarly journals Study on Esculetin to reduce cardiotoxicity induced by Doxorubicin

2021 ◽  
Vol 5 (1) ◽  
pp. 70-73
Author(s):  
Xiao Li ◽  
Xiaolei Yu ◽  
Fan Xu ◽  
Qingshan Li ◽  
Xiao Xu
Keyword(s):  
Flow Cytometry ◽  
Protein Expression ◽  
Caspase 3 ◽  
Intervention Group ◽  
Control Group ◽  
Group Model ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Model Group ◽  
Group Flow

Objective: To investigate the protective effects and mechanisms of esculetin(Esc) on H9C2 cells injury induced by doxorubicin (DOX).  Methods: H9C2 cells were cultured and divided into control group, model (DOX) group and intervention (ESC + DOX) group. Flow cytometry was used to detect apoptosis of H9C2 cells and reactive oxygen (ROS) level in H9C2 cells; Western blotting to detect the cleaved Caspase-3, cleaved PARP, bid and Bcl-2 protein expression in H9C2 cells.  Results: The number of apoptosis and ROS level of H9C2 cells in the model group, the expression of cleaved Caspase-3, cleaved PARP and Bid protein in the model group were obviously higher than control group; and the Bcl-2 protein expression was obviously lower (P < 0.05).The number of apoptosis and ROS level, cleaved Caspase-3, cleaved PARP and Bid protein expression in H9C2 cells in intervention group were obviously lower than model group;the Bcl-2 protein expression was obviously higher (P< 0.05).  Conclusion: Esculetin can reduce the cardiotoxicity induced by doxorubicin by reducing apoptosis and ROS level. 

Effect of Proteasome Inhibitor (Bortezomib) on the Intracellular Level of NF-κBÃ, Â AIκB and P-Gp and the Rate of Apoptosis in Chemotherapy Resistant Myeloid Leukemia Cell Line K562 Induced by Daunorubicin

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3979-3979
Author(s):  
Aijun Liao ◽  
Beibei Fu ◽  
Zhuogang Liu
Keyword(s):  
Flow Cytometry ◽  
Drug Resistance ◽  
Western Blot ◽  
Cell Line ◽  
Proteasome Inhibitor ◽  
Myeloid Leukemia ◽  
Single Agent ◽  
Dependent Manner ◽  
Intracellular Level ◽  
Apoptosis Rate

Abstract Background: NF-κb is a transcription factor in eukaryotic cells that binds to inhibitor protein κB (IκB) in the cytoplasm. Once stress responses occur, IκB is phosphorylated and degraded by the proteasome. Upon dissociation with IκB, activated NF-κB enters the nucleolus and induces the expression of mdr1. MDR-1 encodes the P-glycoprotein (P-gp), which is an ATP-dependent drug efflux pump which lowers intracellular drug concentration resulting in drug resistance. Bortezomib (VELCADE®) is an anti-cancer drug that is a first-in-class proteasome inhibitor and is indicated in treatment of multiple myeloma (MM) patients. However, its role in myeloid leukemia therapy, is still being evaluated. In this study, we observed the effect of bortezomib on the expression of NF-κB AIκB and P-gp in daunorubicin (DNR) resistant cell line K562/DNR, a myeloid cell line; we also discussed the molecular mechanism and functional characteristics of reversing resistance by bortezomib and provided experimental basis to overcome multi-drug resistance in myeloid leukemia. Methods: Resistance of cell line will be evaluated by MTT; After treating K562/DNR for 36h with DNR (100‚•g/ml) alone or combined with bortezomib at different concentration (0.4 mg/L A4 mg/L or 40 mg/L), the expression levels of NF-κB AIκB and P-gp, the activity of NF-κB p65 and the apoptosis rates of cells will be measured by Western blot followed by ELISA and flow cytometry, respectively. After treating K562/DNR for 12h, 24h and 36h with DNR (100 mg/ml) alone or combined with bortezomib (4 mg/L), the same indexes will also be measured; Statistical analysis: With SPSS software, the two group means were compared by t-test and the two sample rates were compared by χ2-test. Results: After treating K562/DNR for 36h with DNR alone or combined with bortezomib at different concentrations, apoptosis rates were measured by flow cytometry. As a single agent, botezomib at concenration of 0.4 mg/L and 4 mg/L did not result in an increase in the rate of apoptosis. However, an increase in apoptosis rate was observed with bortezomib 40 mg/L. In contrast, a combination of DNR and bortezomib resulted in significant increases in apoptosis rate at all doses of bortezomib. Moreover, a dose response was observed. After treating K562/DNR for 12h A24h and 36h with DNR alone or combined with bortezomib, we utilized Western blot to assess the intracellular level of NF-κB AP-gp and IκB. Compared with negative control, DNR as a single agent increased the level of NF-κB AP-gp and decreased the level of IκB. After the addition of bortezomib, the level of NF-κB AP-gp decreased while IκB level increased; furthermore, the effect increased by prolonging the treating time. Conclusion: Based on our observations bortezomib may reverse drug resistance of K562/DNR cell line to DNR. Under optimized conditions, the effect of reversing resistance follows a dose-dependent manner and a time-dependent manner and increases with increasing the concentrations of bortezomib and duration of cellular exposure.

Arsenic Trioxide Induces Platelet Apoptosis

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 5149-5149
Author(s):  
Yicun Wu ◽  
Jin Dai ◽  
Weilin Zhang ◽  
Rong Yan ◽  
Changgeng Ruan ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Western Blot ◽  
Arsenic Trioxide ◽  
Caspase 3 ◽  
Conflicts Of Interest ◽  
Pulmonary Haemorrhage ◽  
Tumour Cells ◽  
Dependent Manner ◽  
Platelet Apoptosis

Abstract Abstract 5149 Objective: Arsenic trioxide, a component of Traditional Chinese Medicine, is known as an effective anticancer drug especially in the treatment of acute promyelocytic leukaemia (APL). APL has emerged as the most curable subtype of acute myeloid leukaemia since the widely use of arsenic trioxide-based chemotherapy. However, recent researches show that thrombocytopenia occurred in 79% of the relapsed or refractory APL patients treated with arsenic trioxide, and part of the APL patients had to be stopped treatment because of catastrophic bleeding, such as intracranial and pulmonary haemorrhage. Thrombocytopenia also occurred in 43% of the myelodysplastic syndrome patients treated with arsenic trioxide. Recently, arsenic trioxide has been proved to have a pro-apoptotic effect on various kinds of nucleated tumour cells or non-tumour cells. The effect of arsenic trioxide on enucleated platelet, however, still remains unclear. The aim of current study is to investigate whether arsenic trioxide induces platelet apoptosis. Methods: Washed platelets (3 × 108/ml) were incubated with different concentrations of arsenic trioxide or vehicle at 37°C for 4 hours. Then, mitochondrial inner transmembrane potential (ΔΨm) and phosphatidylserine (PS) exposure were tested by flow cytometry. In the mean time, the treated platelets were analyzed by western blot for the expression levels of pro-apoptotic protein (Bax), and anti-apoptotic proteins (Bcl-2 and Bcl-XL). Activation of caspase-3 was also examined by western blot using an anti-caspase-3 antibody. Results: ΔΨm depolarization and PS exposure were dose-dependently induced in platelets incubated with different concentrations (2 uM, 4 uM, 8 uM, 16 uM) of arsenic trioxide as detected by flow cytometry, and the lowest concentration of arsenic trioxide incurring ΔΨm depolarization and PS exposure was 4 umol/L. Simultaneously, arsenic trioxide induced up-regulation of Bax and down-regulation of Bcl-2 and Bcl-XL in a dose-dependent manner. Furthermore, 17 kD cleaved caspase-3 fragments were dose-dependently induced in platelets treated with different concentrations of arsenic trioxide indicating that caspase-3 was activated by arsenic trioxide. Conclusions: Taken together, the data indicate that arsenic trioxide induces platelet apoptosis in vitro, which might suggest a novel pathogenic mechanism of thrombocytopenia in the patients who treated with arsenic trioxide. Disclosures: No relevant conflicts of interest to declare.

Arsenic Trioxide Induces Platelet Apoptosis

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4738-4738
Author(s):  
Yicun Wu ◽  
Jin Dai ◽  
Weilin Zhang ◽  
Rong Yan ◽  
Yiwen Zhang ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Platelet Aggregation ◽  
Western Blot ◽  
Arsenic Trioxide ◽  
Caspase 3 ◽  
Specific Inhibitor ◽  
Tumour Cells ◽  
Therapeutic Dosage ◽  
Platelet Apoptosis

Background Arsenic trioxide (ATO), a component of Traditional Chinese Medicine, is known as an effective anticancer drug especially in the treatment of acute promyelocytic leukaemia (APL). APL has emerged as the most curable subtype of acute myeloid leukaemia since the widely use of arsenic trioxide-based chemotherapy. However, recent researches showed that thrombocytopenia occurred in 79% of the relapsed or refractory APL patients treated with arsenic trioxide, and part of the APL patients had to be stopped treatment because of catastrophic bleeding, such as intracranial and pulmonary haemorrhage. Thrombocytopenia also occurred in 43% of the myelodysplastic syndrome patients treated with arsenic trioxide. Recently, arsenic trioxide has been proved to have a pro-apoptotic effect on various kinds of nucleated tumour cells or non-tumour cells. The effect of ATO on enucleated platelet, however, still remains unclear. The aim of current study is to investigate whether ATO induces platelet apoptosis. Methods Washed platelets (3 × 108/ml) were incubated with different concentrations of ATO or vehicle at 37°C for 4 hours. Then, mitochondrial inner transmembrane potential (ΔΨm), phosphatidylserine (PS) exposure, P-selection and PAC-1 binding were tested by flow cytometry. In the mean time, the treated platelets were analyzed by western blot for the expression levels of pro-apoptotic protein (Bax), and anti-apoptotic proteins (Bcl-2 and Bcl-XL). Activation of caspase-3 and c-jun NH2-terminal kinase (JNK) was also examined by western blot. To test whether inhibition of JNK can attenuate ATO-induced platelet apoptosis, JNK specific inhibitor dicumarol was used and ΔΨm was analysis by flow cytometry. For platelet aggregation analysis, PRP was incubated with ATO (2 μM) for 1 hr and then subjected to platelet aggregation assay by collagen. To further investigate whether ATO incurs thrombocytopenia in vivo, clinical therapeutic dosage of ATO (or vehicle (0.9% NS) control) was intraperitoneally injected into C57 mice, and the numbers of circulating platelets were counted. Results and Conclusions ATO dose-dependently induces depolarization of mitochondrial inner ΔΨm, up-regulation of Bax and down-regulation of Bcl-2 and Bcl-XL, caspase-3 activation, and PS exposure in platelets. ATO did not induce surface expression of P-selectin and PAC-1 binding, whereas, obviously reduced collagen-induced platelet aggregation. ATO dose-dependently induced JNK activation, and JNK specific inhibitor dicumarol obviously reduced ATO-induced ΔΨm depolarization in platelets. Clinical therapeutic dosage of ATO was intraperitoneally injected into C57 mice, and the numbers of circulating platelets were significantly reduced after 12 and 24 hours of injection. Taken together, the data demonstrate that ATO induces caspase-dependent apoptosis via mitochondria-mediated intrinsic pathway in platelets. ATO does not incur platelet activation, whereas, it not only impairs platelet function but also incurs thrombocytopenia in vivo, suggesting the possible pathogenesis of thrombocytopenia in patients treated with ATO. Disclosures: No relevant conflicts of interest to declare.

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