Inhibition of PI3K/AKT signaling pathway prevents blood-induced heterotopic ossification of the injured tendon.

Objective: It is a common clinical phenomenon that blood infiltrates into the injured tendon caused by sports injuries, accidental injuries, and surgery. However, the role of blood infiltration into the injured tendon has not been investigated. Methods: A blood-induced rat model was established and the impact of blood infiltration on inflammation and HO of the injured tendon was assessed. Cell adhesion, viability, apoptosis, and gene expression were measured to evaluate the effect of blood treatment on tendon stem/progenitor cells (TSPCs). Then RNA-seq was used to assess transcriptomic changes in tendons in a blood infiltration environment. At last, the small molecule drug PI3K inhibitor LY294002 was used for in vivo and in vitro HO treatment. Results: Blood caused acute inflammation in the short term and more severe HO in the long term. Then we found that blood treatment increased cell apoptosis and decreased cell adhesion and tenonic gene expression of TSPCs. Furthermore, blood treatment promoted osteochondrogenic differentiation of TSPCs. Next, we used RNA-seq to find that the PI3K/AKT signaling pathway was activated in blood-treated tendon tissues. By inhibiting PI3K with a small molecule drug LY294002, the expression of osteochondrogenic genes was markedly downregulated while the expression of tenonic genes was significantly upregulated. At last, we also found that LY294002 treatment significantly reduced the tendon HO in the rat blood-induced model. Conclusion: Our findings indicate that the upregulated PI3K/AKT signaling pathway is implicated in the aggravation of tendon HO. Therefore, inhibitors targeting the PI3K/AKT pathway would be a promising approach to treat blood-induced tendon HO.

Conservative treatment of hepatic portal vein gas after transarterial chemoembolization treatment for liver metastasis of postoperative esophageal cancer: a case report.

Background: Hepatic portal vein gas (HPVG), which is a rare clinical manifestation, is usually considered a sign of critical illness. If the treatment is not timely, it will lead to intestinal ischemia, intestinal necrosis, and even death. There is still no consensus on whether to adopt surgical or conservative treatment for HPVG. Herein, we report a rare case of conservative treatment of HPVG after transarterial chemoembolization (TACE) treatment in a patient with liver metastasis of postoperative esophageal cancer, who received long-term enteral nutrition (EN). Case Description: A 69-year-old male patient, who had undergone surgery for esophageal cancer, needed long-term use of jejunal feeding tube implantation for enteral nutritional support due to postoperative complications. About 9 months after the operation, multiple metastases of the liver were detected. To control the progress of the disease, TACE was conducted. EN was restored on the second day after TACE, and the patient was discharged on the fifth day. On the night of discharge, the patient suddenly experienced abdominal pain, nausea, and vomiting. Abdominal computed tomography (CT) showed that the abdominal intestinal lumen was obviously dilated, liquid and gas plane shadowing was visible, and gas was visible in the portal vein and its branches. The physical examination showed that peritoneal irritation was present, and bowel sounds were active. Blood routine examination showed an increase in neutrophil and neutrophil. Symptomatic treatment, including gastrointestinal decompression, anti-infection, and parenteral nutritional support, was provided. On the third day after the presentation of HPVG, abdominal CT reexamination showed that HPVG had disappeared and the intestinal obstruction was relieved. Repeated blood routine shows a decrease in neutrophil and neutrophil. Conclusions: Elderly patients who require long-term EN support should avoid early EN support after TACE, as this can prevent intestinal obstruction and HPVG. If the patient suddenly experiences abdominal pain after TACE, CT scan should be performed in a timely manner to determine whether there is intestinal obstruction and HPVG. If the above type of patient experiences HPVG, conservative treatments such as early gastrointestinal decompression, fasting, and anti-infection treatment can be provided first without high-risk factors.

Fasudil inhibits hepatic artery spasm by repressing the YAP/ERK/ ETA/ETB signaling pathway via inhibiting ROCK activation.

OBJECTIVE: To explore the effect of Fasudil on HA spasm and its underlying mechanism. METHODS: Rabbits were divided into Sham, Fasudil, and Model groups for experiments. Fasudil was injected into the left medial lobe of the rabbit liver using a 16G lumbar puncture needle through the laparotomic route. The spasm model was established by inserting the catheter sheath into the femoral arteries of rabbits, followed by celiac artery angiography and left HA catheterization with a micro-catheter. Next, the GSE60887 and GSE37924 datasets concerning Fasudil treatment were analyzed. Moreover, immunofluorescence staining was conducted for YAP1 and α-SMA. Finally, Western blotting was performed to examine the expressions of YAP1, ROCK, ERK1/2, ETA, and ETB. RESULTS: Fasudil could relieve HA spasm. The Go and KEGG pathway analyses revealed that the MAPK signaling pathway and the Hippo signaling pathway were enriched in vasospasm. Besides, GSEA revealed that ROCK was functionally enriched in the MAPK and Hippo signaling pathways. Co-expression analysis revealed that MAPK1 was significantly correlated with YAP1 and MYC, and YAP1 was significantly correlated with ETA and ETB. It was manifested in the results of immunofluorescence staining that the YAP1-positive fluorescence area was significantly decreased after Fasudil treatment. Moreover, Western blotting results showed that Fasudil decreased the expressions of YAP1, RhoA, ROCK, ETA, ETB, and p-ERK1/2. In addition, in-vitro Western blotting revealed that Fasudil suppressed the YAP/ERK/ETA/ETB signaling pathway in the case of HA spasm by inhibiting ROCK activation. CONCLUSIONS: Fasudil ameliorates HA spasm through suppressing the YAP/ERK/ETA/ETB signaling pathway and the ROCK activation.

Free or fixed state of nHAP differentially regulates hBMSC morphology and osteogenesis through the valve role of ITGA7.

Nano-hydroxyapatite (nHAP) has been widely used in bone repair as an osteo-inductive and naturally-occurring material. However, the optimal applied form of nHAP and the underlying mechanisms involved remain unclear. Herein, to investigate into these, a range of corresponding models were designed, including three applied forms of nHAP (Free, Coating and 3D) that belong to two states (Free or fixed). The results indicate that when fixed nHAP was applied in the 3D form, optimal osteogenesis was induced in human bone marrow stem cells (hBMSCs) with increased bone volume via integrin α7 (ITGA7)-mediated upregulation of the PI3K-AKT signaling pathway, while contrary results were observed with free nHAP. Ectopic osteogenesis experiments in mice subcutaneous transplantation model further confirmed the different tendencies of ITGA7 expression and osteogenesis of hBMSCs in free and fixed states of nHAP. Our results revealed that the two states of nHAP play a different regulatory role in cell morphology and osteogenesis through the valve role of ITGA7, providing cues for better application of nanoparticles and a potential new molecular target in bone tissue engineering.

Nephroprotective effect of magnesium isoglycyrrhizinate against arsenic trioxide-induced acute kidney damage in mice.

Magnesium isoglycyrrhizinate (MgIG) has anti-inflammatory, antioxidative, antiviral and anti-hepatotoxic effects. However, protective effects of MgIG against renal damage caused by arsenic trioxide (ATO) have not been reported. The present study aimed to clarify the protective function of MgIG on kidney damaged induced by ATO. Other than the control group and the group treated with MgIG alone, mice were injected intraperitoneally with ATO (5 mg/kg/day) for 7 days to establish a mouse model of kidney damage. On the 8th day, blood and kidney tissue were collected and the inflammatory factors and antioxidants levels in the kidney tissue and serum were measured. The expression of protein levels of caspase-3, Bcl-2, Bax, Toll-like receptor-4 (TLR4) and nuclear factor-κB (NF-κB) were determined via western blot analysis. In the renal tissue of mice, ATO exposure dramatically elevated markers of oxidative stress, apoptosis and inflammation. However, MgIG could also restore the activities of urea nitrogen and creatinine to normal levels, decrease the malondialdehyde level and reactive oxygen species formation and increase superoxide dismutase, catalase and glutathione activities. MgIG also ameliorated the morphological abnormalities generated by ATO, reduced inflammation and apoptosis and inhibited the TLR4/NF-κB signaling pathway. In conclusion, MgIG may mitigate ATO-induced kidney damage by decreasing apoptosis, oxidative stress and inflammation and its mechanism may be connected to the inhibition of TLR4/NF-κB signaling.

Exploring the Mechanism of Danshensu in the Treatment of Doxorubicin-Induced Cardiotoxicity Based on Network Pharmacology and Experimental Evaluation.

Background: Doxorubicin (DOX) is one of the most effective chemotherapeutic agents available; however, its use is limited by the risk of serious cardiotoxicity. Danshensu (DSS), an active ingredient in Salvia miltiorrhiza, has multiple cardioprotective effects, but the effect of DSS on DOX-induced cardiotoxicity has not been reported. Objectives: Predicting the targets of DOX-induced cardiotoxicity and validating the protective effects and mechanisms of DSS. Methods: (1) Using methods based on network pharmacology, DOX-induced cardiotoxicity was analyzed by data analysis, target prediction, PPI network construction and GO analysis. (2) The cardiotoxicity model was established by continuous intraperitoneal injection of 15 mg/kg of DOX into mice for 4 days and the protective effects and mechanism were evaluated by treatment with DSS. Results: The network pharmacology results indicate that CAT, SOD, GPX1, IL-6, TNF, BAX, BCL-2, and CASP3 play an important role in this process, and Keap1 is the main target of DOX-induced cardiac oxidative stress. Then, based on the relationship between Keap1 and Nrf2, the Keap1-Nrf2/NQO1 pathway was confirmed by animal experiments. In the animal experiments, by testing the above indicators, we found that DSS effectively reduced oxidative stress, inflammation, and apoptosis in the damaged heart, and significantly alleviated the prolonged QTc interval caused by DOX. Moreover, compared with the DOX group, DSS elevated Keap1 content and inhibited Nrf2, HO-1, and NQO1. Conclusion: The results of network pharmacology studies indicated that Keap1-Nrf2/NQO1 is an important pathway leading to DOX-induced cardiotoxicity, and the results of animal experiments showed that DSS could effectively exert anti-oxidative stress, anti-inflammatory and anti-apoptotic therapeutic effects on DOX-induced cardiotoxicity by regulating the expression of Keap1-Nrf2/NQO1.

Liquiritigenin protects against arsenic trioxide-induced liver injury by inhibiting oxidative stress and enhancing mTOR-mediated autophagy.

Liquiritigenin (LQ) has protective effects against various hepatotoxicities. However, its specific role on arsenic trioxide (ATO)-induced hepatotoxicity and the related biomolecular mechanisms remain unclear. The purpose of this study is to explore the protective actions of LQ on ATO-induced hepatotoxicity and its biomolecular mechanisms in mice. LQ was administered orally at 20 and 40 mg/kg per day for seven consecutive days with an intraperitoneal injection of ATO (5 mg/kg). Liver injury was induced by ATO and was alleviated by treatment with LQ as reflected by reduced histopathological damage of liver and decreased serum ALT, AST, and ALP levels. The generation of intracellular ROS induced by ATO was attenuated after LQ treatment. The levels of SOD, CAT, and GSH were elevated with LQ administration while MDA levels decreased. LQ mitigated elevated TNF-α and IL-6 levels as well as the hepatic mitochondrial damage caused by ATO. Moreover, LQ upregulated the expression of LC3-II and enhanced autophagy in the liver of ATO-induced mice. Further studies indicated that LQ significantly suppressed the expression of p-PI3K, p-AKT, and p-mTOR in ATO-induced mice. In conclusion, our findings show that LQ protects against ATO-induced hepatotoxicity due to its antioxidant and anti-inflammatory activities and enhancement of autophagy mediated by the PI3K/AKT/mTOR signaling pathway in mice.

Investigation of the ameliorative effects of baicalin against arsenic trioxide-induced cardiac toxicity in mice.

Baicalin (BA), a kind of flavonoids compound, comes from Scutellaria baicalensis Georgi (a kind of perennial herb) and has beneficial effects on the cardiovascular system through anti-oxidant, anti-inflammation, and anti-apoptosis actions. However, the therapeutic effects and latent mechanisms of BA on arsenic trioxide (ATO)-induced cardiac toxicity has not been reported. The present research was performed to explore the effects and mechanisms of BA on ATO-induced heart toxicity. Male Kunming mice were treated with ATO (7.5 mg/kg) to induce cardiac toxicity. After the mice received ATO, BA (50 and 100 mg/kg) was administered for estimating its cardioprotective effects. Statistical data demonstrated that BA treatment alleviated electrocardiogram abnormalities and pathological injury caused by ATO. BA could also lead to recovery of CK and LDH activities to normal range and cause a decrease in MDA levels and ROS generation, augmentation of SOD, CAT, and GSH activities. We also found that BA caused a reduction in the expression of proinflammatory cytokines, such as TNF-α and IL-6. Moreover, BA attenuated ATO-induced apoptosis by promoting the expression of Bcl-2 and suppressing the expression of Bax and caspase-3. TUNEL test result demonstrated BA caused impediment of ATO-induced apoptosis. Furthermore, BA treatment suppressed the high expression of TLR4, NF-κB and P-NF-κB caused by ATO. In conclusion, these results indicate that BA may alleviate ATO-induced cardiac toxicity by restraining oxidative stress, apoptosis, and inflammation, and its mechanism would be associated with the inhibition of the TLR4/NF-κB signaling pathway.

Structural and physiological changes of the human body upon SARS-CoV-2 infection.

Since December 2019, the novel coronavirus (severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)) has spread to many countries around the world, developing into a global pandemic with increasing numbers of deaths reported worldwide. To data, although some vaccines have been developed, there are no ideal drugs to treat novel coronavirus pneumonia (coronavirus disease 2019 (COVID-19)). By examining the structure of the coronavirus and briefly describing its possible pathogenesis based on recent autopsy reports conducted by various teams worldwide, this review analyzes the possible structural and functional changes of the human body upon infection with SARS-CoV-2. We observed that the most prominent pathological changes in COVID-19 patients are diffuse alveolar damage (DAD) of the lungs and microthrombus formation, resulting in an imbalance of the ventilation/perfusion ratio and respiratory failure. Although direct evidence of viral infection can also be found in other organs and tissues, the viral load is relatively small. The conclusion that the injuries of the extra-pulmonary organs are directly caused by the virus needs further investigation.

ADAMTS8 Inhibits Progression of Esophageal Squamous Cell Carcinoma.

A disintegrin and metallopeptidase with thrombospondin motifs (ADAMTSs), which is frequently dysregulated in cancers and is involved in carcinogenesis and cancer progression. The present study identified that ADAMTS8 expression is downregulated in esophageal squamous cell carcinoma (ESCC) tissues when compared with nontumor tissue. The expression of ADAMTS8 is closely associated with clinical stage and lymph node metastasis in patients with ESCC. Furthermore, functional studies have shown that ADAMTS8 overexpression could reduce abilities of proliferation, migration, and invasion and promote apoptosis of ESCC cells. Meanwhile, monocyte chemotactic protein-1 and interleukin-6 are markedly deregulated by ADAMTS8 overexpression. Consistently, in vivo data showed that ADAMTS8 overexpression led to a reduction in tumor growth. These results indicate that altering ADAMTS8 expression could modify the outcomes of ESCC by inhibiting cell proliferation and invasion, while promoting the apoptosis of ECSS cells. Thus, ADAMTS8 represents a potential therapeutic target for ESCC therapy.

Cardioprotective Effect of Monoammonium Glycyrrhizinate Injection Against Myocardial Ischemic Injury in vivo and in vitro: Involvement of Inhibiting Oxidative Stress and Regulating Ca2+ Homeostasis by L-Type Calcium Channels.

PURPOSE: Monoammonium glycyrrhizinate (MAG) is an aglycone of glycyrrhizin that is found in licorice and is often used clinically as an injection to treat liver diseases. However, the effect of MAG injection on cardiac function and its possible cellular mechanisms remain unclear. We explored the protective effects of MAG against myocardial ischemic injury (MII) induced by isoproterenol (ISO), as well as the cellular mechanisms via molecular biology techniques and patch-clamp recording. METHODS: A rat model of myocardial ischemia injury was induced by administering ISO (85 mg/kg) subcutaneously for 2 consecutive days. ECG, cardiac functional parameters, CK and LDH levels, SOD and GSH activities, MDA concentration, histological myocardium inspection, mitochondria ultrastructure changes, intracellular calcium concentrations were observed. Influences of MAG on ICa-L and contraction in isolated rat myocytes were observed by the patch-clamp technique. RESULTS: MAG reduced damage, improved cardiac morphology, inhibited oxidative stress, decreased the generation of reactive oxygen species, and decreased intracellular Ca2+ concentration. Exposure of the rats' ventricular myocytes to MAG resulted in a concentration-dependent reduction in L-type calcium currents (ICa-L). MAG reduced ICa-L in a consistent and time-dependent fashion with a semi-maximal prohibitive concentration of MAG of 14 µM. MAG also shifted the I-V curve of ICa-L upwards and moved the activation and inactivation curves of ICa-L to the left. CONCLUSION: The findings indicate that MAG injection exerts a protective influence on ISO-induced MII by inhibiting oxidative stress and regulating Ca2+ homeostasis by ICa-L.

Cardioprotective effects of glycyrrhizic acid involve inhibition of calcium influx via L-type calcium channels and myocardial contraction in rats.

Glycyrrhizic acid (GA) is one of the main active components in licorice and has often been reported to have cardioprotective effects. However, the underlying cellular mechanisms remain unclear. The aim of this study is to verify the protective effects of GA against isoproterenol (ISO)-induced myocardial ischemia injury in rats. Another aim is to explore the cellular mechanisms based on the L-type Ca2+ channel, myocardial cell contraction, and intracellular Ca2+ ([Ca2+]i) transient. The results show that GA reduced the ST segment elevation, decreased the heart rate, prevented ISO-induced QT-interval shortening, improved heart morphology, and decreased the activity of CK and LDH. GA blocked ICa-L in a dose-dependent manner. The concentration for 50% of the maximal effect (EC50) of GA was 145.54 µg/mL, and the maximal inhibition was 47.43 ± 0.75% at 1000 µg/mL. However, GA did not affect the dynamical properties of the Ca2+ channel. GA reversibly reduced the amplitude of cell contraction in a dose-dependent manner and slowed down its deflection and recovery, as well as the [Ca2+]i transient. The data demonstrate that GA inhibits L-type Ca2+ channels, decreases the [Ca2+]i transient, and shows a negative cardiac inotropic effect in the ventricular myocardial cells of adult rats. It also protects the myocardia from ischemia injury induced by ISO.

Role of forward and reverse signaling in Eph receptor and ephrin mediated cell segregation.

Eph receptor and ephrin signaling has a major role in segregating distinct cell populations to form sharp borders. Expression of interacting Ephs and ephrins typically occurs in complementary regions, such that polarised activation of both components occurs at the interface. Forward signaling through Eph receptors can drive cell segregation, but it is unclear whether reverse signaling through ephrins can also contribute. We have tested the role of reverse signaling, and of polarised versus non-polarised activation, in assays in which contact repulsion drives cell segregation and border sharpening. We find that polarised forward signaling drives stronger segregation than polarised reverse signaling. Nevertheless, reverse signaling contributes since bidirectional Eph and ephrin activation drives stronger segregation than unidirectional forward signaling alone. In contrast, non-polarised Eph activation drives little segregation. We propose that although polarised forward signaling is the principal driver of segregation, reverse signaling enables bidirectional repulsion which prevents mingling of each population into the other.

Enhanced electrochemical performance of CuCo2S4/carbon nanotubes composite as electrode material for supercapacitors.

CuCo2S4 is regarded as a promising electrode material for supercapacitor, but has inferior conductivity and poor cyclic stability which restrict its wide-range applications. In this work, hierarchically hybrid composite of CuCo2S4/carbon nanotubes (CNTs) was synthesized using a facile hydrothermal and sulfuration process. The embedded CNTs in the CuCo2S4 matrix provided numerous effective paths for electron transfer and ion diffusion, and thus promoted the faradaic reactions of the CuCo2S4 electrode in the energy storage processes. The CuCo2S4/CNTs-3.2% electrode exhibited a significantly increased specific capacitance of 557.5 F g-1 compared with those of the pristine CuCo2S4 electrode (373.4 F g-1) and CuO/Co3O4/CNTs-3.2% electrode (356.5 F g-1) at a current density of 1 A g-1. An asymmetric supercapacitor (ASC) was assembled using the CuCo2S4/CNTs-3.2% as the positive electrode and the active carbon as the negative electrode, which exhibited an energy density of 23.2 Wh kg-1 at a power density of 402.7 W kg-1. Moreover, the residual specific capacitance of this ASC device retained 85.7% of its original value after tested for 10,000 cycles, indicating its excellent cycle stability.

Ultrafast Response/Recovery and High Selectivity of the H2S Gas Sensor Based on α-Fe2O3 Nano-Ellipsoids from One-Step Hydrothermal Synthesis.

Ultrafast response/recovery and high selectivity of gas sensors are critical for real-time and online monitoring of hazardous gases. In this work, α-Fe2O3 nano-ellipsoids were synthesized using a facile one-step hydrothermal method and investigated as highly sensitive H2S-sensing materials. The nano-ellipsoids have an average long-axis diameter of 275 nm and an average short-axis diameter of 125 nm. H2S gas sensors fabricated using the α-Fe2O3 nano-ellipsoids showed excellent H2S-sensing performance at an optimum working temperature of 260 °C. The response and recovery times were 0.8 s/2.2 s for H2S gas with a concentration of 50 ppm, which are much faster than those of H2S gas sensors reported in the literature. The α-Fe2O3 nano-ellipsoid-based sensors also showed high selectivity to H2S compared to other commonly investigated gases including NH3, CO, NO2, H2, CH2Cl2, and ethanol. In addition, the sensors exhibited high-response values to different concentrations of H2S with a detection limit as low as 100 ppb, as well as excellent repeatability and long-term stability.

Magnesium isoglycyrrhizinate ameliorates doxorubicin-induced acute cardiac and hepatic toxicity via anti-oxidant and anti-apoptotic mechanisms in mice.

The present study investigated the effects and potential mechanisms of action of magnesium isoglycyrrhizinate (MgIG) in doxorubicin (DOX)-treated mice. Histopathological analysis and western blot analysis were conducted in the liver and heart tissues and biochemical analysis of the serum was performed. The results revealed that MgIG (10, 20 and 40 mg/kg/day) could protect the structure and functions of the liver and heart by inhibiting the activities of the myocardial enzymes creatine kinase (CK), CK-MB and lactate dehydrogenase and the hepatic-specific enzymes aspirate aminotransferase and alanine aminotransferase, increasing the activities of the antioxidants superoxide dismutase and glutathione peroxidase, and inhibiting cellular apoptosis induced by DOX (30 mg/kg). These results demonstrate that inhibiting lipid peroxidation and reducing myocardial and hepatocyte apoptosis may be one of the mechanisms by which MgIG exhibits hepatoprotective and cardioprotective effects in DOX-treated mice.

Cell segregation and border sharpening by Eph receptor-ephrin-mediated heterotypic repulsion.

Eph receptor and ephrin signalling has a major role in cell segregation and border formation, and may act through regulation of cell adhesion, repulsion or tension. To elucidate roles of cell repulsion and adhesion, we combined experiments in cell culture assays with quantitations of cell behaviour which are used in computer simulations. Cells expressing EphB2, or kinase-inactive EphB2 (kiEphB2), segregate and form a sharp border with ephrinB1-expressing cells, and this is disrupted by knockdown of N-cadherin. Measurements of contact inhibition of locomotion reveal that EphB2-, kiEphB2- and ephrinB1-expressing cells have strong heterotypic and weak homotypic repulsion. EphB2 cells have a transient increase in migration after heterotypic activation, which underlies a shift in the EphB2-ephrinB1 border but is not required for segregation or border sharpening. Simulations with the measured values of cell behaviour reveal that heterotypic repulsion can account for cell segregation and border sharpening, and is more efficient than decreased heterotypic adhesion. By suppressing homotypic repulsion, N-cadherin creates a sufficient difference between heterotypic and homotypic repulsion, and enables homotypic cohesion, both of which are required to sharpen borders.

Decitabine for the treatment of atypical chronic myeloid leukemia: A report of two cases.

Atypical chronic myeloid leukemia (aCML) is a hematopoietic stem/progenitor cell disorder, predominantly involving neutrophils. At present, a limited number of studies regarding the treatment of aCML have been published, and the therapies that are currently available exhibit unsatisfactory outcomes. In the present study, the cases of two aCML patients treated with decitabine (DCA) therapy who achieved remission are presented. A 48-year-old male, who presented with fatigue and a cough that had lasted two months, and a 69-year-old male who presented with dizziness, fatigue and shortness of breath with exercise, were diagnosed with aCML following bone marrow examination, flow cytometry and chromosome banding analysis. The two patients were treated with four cycles of DCA chemotherapy (20 mg/m2, days 1-5) and remission was achieved in each patient. The present study evaluated the clinical manifestations, diagnostic criteria and relevant treatment regimens of aCML, which may provide insights for the treatment of affected patients. Routine blood and bone marrow examinations were performed weekly prior to each cycle. Symptoms were relieved in both patients after the first cycle and the two patients were followed up for 3 months after completion of the final cycle. The findings of the current case report indicate that DCA may present an efficacious treatment for aCML.