Saikosaponin A Inhibits Growth of Human Bladder Carcinoma T24 and 5637 Cells Both in Vitro and in Vivo.

Saikosaponin A (SSA)-a natural compound extracted from Radix bupleuri-possesses antitumor properties in several types of carcinomas. However, the role of SSA on bladder cancer and the mechanisms remain unclear. In this study, we have described the effect of SSA on human bladder cancer cell lines T24 and 5637 in the context of the regulation of mitochondrial pathways of apoptosis. In vitro, the Cell Counting Kit-8 (CCK-8) assay and cell wound healing assays were used to determine the proliferative effect of SSA treatment. Flow cytometry and Western blotting were performed to evaluate the apoptosis and related mechanisms. To further confirm that apoptosis is mediated through Caspase activation, Hoechst 33258 fluorescence staining assay was done after cells were treated with SSA and caspase inhibitor-Z-VAD-FMK. In vivo, an orthotopic xenograft mice model was adopted to evaluate the effect of SSA. The tumors were analyzed by hematoxylin-eosin (H&E) staining, immunohistochemical analysis, and Western blotting. In vitro, the results with CCK-8 assay showed obvious SSA-induced suppression in cell growth in a dose- and time-dependent manner. Flow cytometry analysis, Hoechst 33258 fluorescence staining assay and the assessment of the changes in the B-cell lymphoma 2 (Bcl-2) family protein expression level revealed that SSA could significantly induce cell apoptosis, which was associated with apoptosis via the mitochondrial pathways. In vivo, the results revealed a reduction in cell proliferation. In conclusion, our data suggest that SSA inhibits the growth of bladder cancer cells by activating the mitochondrial apoptosis pathway and inducing cell apoptosis.

CHARACTERISTICS AND FACTORS INFLUENCING UNPROTECTED ANAL INTERCOURSE AMONG MEN WHO HAVE SEX WITH MEN IN FUYANG, CHINA.

Men who have sex with men (MSM) are at risk for contracting hu- man immunodeficiency virus (HIV) infection. The objective of this study was to explore the characteristics and factors influencing unprotected anal intercourse (UAI) among MSM in Fuyang, China in order to develop an intervention program to prevent the spread of HIV infection among MSM. We conducted this cross sectional study among 413 MSM in 2013. Participants completed an interviewer- administered questionnaire and were tested for HIV and syphilis infections. Three hundred fifty of 413 subjects reported sexual activity with a male partner during the previous 6 months; of these 27(7.7%) had unprotected sex. Forty-four subjects had sex with a female partner during the previous 6 months; of these 25 (58.1%) had unprotected sex. The frequency of having unprotected sex with a female was significantly greater than with a male (χ2 = 84.52, p < 0.001). Multivariate logistic analysis showed education level (OR = 0.45, p = 0.003), length of time of current residence (OR = 0.47, p = 0.014), knowledge about HIV infection (OR = 0.09, p = 0.022) and integrated interventions (OR = 0.32, p < 0.001) were all significantly associated with UAI. High-risk sex behavior was common among the study population. A targeted interventions needs to be developed urgently.

A Qualitative Study on Nutritional Awareness Among Parents of Pediatric Recipients of Liver or Kidney Transplants.

Objective: The primary aim of this study was to examine the extent of nutritional awareness concerning dietary requisites within a cohort comprising pediatric recipients of liver and kidney transplants, along with their respective caregivers. The overarching goal was to establish a foundation for enhancing the dietary nutrition of this specific population. Methods: This was a qualitative research study, involving in-depth interviews and subsequent qualitative data analysis. Our sample included pediatric patients in a specific age range who had undergone a liver or kidney transplant, as well as their parents. The data analysis technique we used was content analysis. Results: The survey focused on knowledge of dietary requirements and restrictions, nutritional needs, and adherence to daily dietary requirements among pediatric patients and their respective caregivers. Approximately 30% of the parents lacked relevant nutritional awareness, 30% relied on a single source for acquiring nutritional knowledge, and 40% expressed a considerable need for nutritional guidance. Our findings revealed a deficiency in the understanding of nutritional and dietary requirements for children who have undergone a liver or kidney transplant. Their nutrient intake was unbalanced, and their dietary habits were irregular, highlighting the need for better nutritional guidance and monitoring. Conclusion: The nutritional awareness and knowledge of dietary requirements among pediatric liver and kidney transplant recipients and their care providers are inadequate. Medical professionals are urged to tackle this concern by imparting comprehensive education to parents regarding the nutritional prerequisites essential for their children post-transplant. This approach empowers parents to implement requisite dietary modifications effectively. Furthermore, healthcare institutions should augment the nutritional proficiency of their medical staff through meticulously structured training initiatives.

Structural abnormality of hepatic glycogen in rat liver with diethylnitrosamine-induced carcinogenic injury.

Growing evidence confirms associations between glycogen metabolic re-wiring and the development of liver cancer. Previous studies showed that glycogen structure changes abnormally in liver diseases such as cystic fibrosis, diabetes, etc. However, few studies focus on glycogen molecular structural characteristics during liver cancer development, which is worthy of further exploration. In this study, a rat model with carcinogenic liver injury induced by diethylnitrosamine (DEN) was successfully constructed, and hepatic glycogen structure was characterized. Compared with glycogen structure in the healthy rat liver, glycogen chain length distribution (CLD) shifts towards a short region. In contrast, glycogen particles were mainly present in small-sized ß particles in DEN-damaged carcinogenic rat liver. Comparative transcriptomic analysis revealed significant expression changes of genes and pathways involved in carcinogenic liver injury. A combination of transcriptomic analysis, RT-qPCR, and western blot showed that the two genes, Gsy1 encoding glycogen synthase and Gbe1 encoding glycogen branching enzyme, were significantly altered and might be responsible for the structural abnormality of hepatic glycogen in carcinogenic liver injury. Taken together, this study confirmed that carcinogenic liver injury led to structural abnormality of hepatic glycogen, which provided clues to the future development of novel drug targets for potential therapeutics of carcinogenic liver injury.

Subsequent maternal sleep deprivation aggravates cognitive impairment by modulating hippocampal neuroinflammatory responses and synaptic function in maternal isoflurane-exposed offspring mice.

INTRODUCTION: Pregnant women may need to undergo non-obstetric surgery under general anesthesia owing to medical needs, and pregnant women frequently experience sleep disturbances during late gestation. Preclinical studies demonstrated that maternal isoflurane exposure (MISO) or maternal sleep deprivation (MSD) contributed to cognitive impairments in offspring. Research studies in mice have revealed that SD can aggravate isoflurane-induced cognitive deficits. However, it remains unclear whether MSD aggravates MISO-induced cognitive deficits in offspring. The purpose of this research was to explore the combined effects of MSD and MISO on offspring cognitive function and the role of neuroinflammation and synaptic function in the process of MSD + MISO. METHODS: Pregnant mice were exposed to 1.4% isoflurane by inhalation for 4 h on gestational day (GD) 14. Dams were then subjected to SD for 6 h (12:00-18:00 h) during GD15-21. At 3 months of age, the offspring mice were subjected to the Morris water maze test to assess cognitive function. Then the levels of inflammatory and anti-inflammatory markers and synaptic function-related proteins were assessed using molecular biology methods. RESULTS: The results of this study demonstrated that MISO led to cognitive dysfunction, an effect that was aggravated by MSD. In addition, MSD exacerbated the maternal isoflurane inhalation, leading to an enhancement in the expression levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor-alpha and a reduction in the hippocampal levels of IL-10, synaptophysin, post-synaptic density-95, growth-associated protein-43, and brain-derived neurotrophic factor. CONCLUSION: Our findings revealed that MSD aggravated the cognitive deficits induced by MISO in male offspring mice, and these results were associated with neuroinflammation and alternations in synaptic function.

Strategy for enhancing second-order nonlinear optical properties of the Pt(II) dithienylethene complexes: substituent effect, π-conjugated influence, and photoisomerization switch.

The second-order nonlinear optical (NLO) properties of a series of Pt(II) dithienylethene (DTE) complexes possessing the reversible photochromic behavior have been investigated by density functional theory (DFT) combined with the analytic derivatives method. The results show that the calculated static first hyperpolarizabilities (ßtot) of the open-ring and closed-ring systems significantly increase in the range of 2.1-4.5 times through strengthening of the electron-withdrawing ability of the substituent R (R = H, CF3, NO2) and an increase of the number of thiophene rings. Moreover, there is a large enhancement of the ßtot values from the open-ring systems to the corresponding closed-ring systems. This efficient enhancement is attributed to the better delocalization of the π-electron system, the more obvious degree of charge transfer, and the larger f(os)/E(gm)(3) (f(os) is the oscillator strength, and E(gm) is the transition energy between the ground and the excited states) values in the closed forms according to the bond length alternation (BLA) and time-dependent density functional theory (TDDFT) calculations. In addition, the dispersion has less influence on the frequency-dependent first hyperpolarizabilities (ßtot(ω)) of the studied systems at the low-frequency area ω (0.000-0.040 au). Our present work would be beneficial for further theoretical and experimental studies on large second-order NLO responses of metal complexes.

[Autophagy expression and its significance in chondrocytes from a degenerate model of human cervical endplate].

OBJECTIVE: To explore the autophagy expression and examine its significance in chondrocytes in a degenerate model of human cervical vertebrae endplate. METHODS: Cartilage endplates were obtained from 48 hospitalized patients with cervical vertebral fracture or dislocation at our hospital between February 2012 to August 2012. They were divided into cervical spondylosis group with cervical spondylotic myelopathy (n = 31) and control group (n = 17).Endplate chondrocytes were isolated by enzyme digestion and cultured in vitro. The cells were stained with toluidine blue and hematoxylin and eosin; laser scanning confocal microscope and monodansylcadaverine (MDC) were used to observe autophagy in endplate chondrocytes; reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of typeIIcollagen and aggrecan and Western blot for the protein of LC3. RESULTS: A degenerative cell model of human cervical endplate chondrocytes was established successfully in vitro. Compared with the common group, the cellular morphologies of degenerative group showed spindle changes. Autophagic body was stained with MDC.Intracellular and perinuclear LC3 protein was detected by laser confocal microscopy. Compared with the control group, the mRNA expressions of aggrecan (0.715 ± 0.194) and typeII collagen (0.628 ± 0.254) markedly decreased (0.845 ± 0.186,0.913 ± 0.254, P < 0.05) and LC3-II/LC3-I declined in cervical spondylosis group. CONCLUSION: Autophagy plays an important pathogenic role in the process of human cervical disc degeneration. And regulating its expression may improve disc degeneration in endplate cartilage cells.

The gut microbial metabolite trimethylamine N-oxide and cardiovascular diseases.

Morbidity and mortality of cardiovascular diseases (CVDs) are exceedingly high worldwide. Researchers have found that the occurrence and development of CVDs are closely related to intestinal microecology. Imbalances in intestinal microecology caused by changes in the composition of the intestinal microbiota will eventually alter intestinal metabolites, thus transforming the host physiological state from healthy mode to pathological mode. Trimethylamine N-oxide (TMAO) is produced from the metabolism of dietary choline and L-carnitine by intestinal microbiota, and many studies have shown that this important product inhibits cholesterol metabolism, induces platelet aggregation and thrombosis, and promotes atherosclerosis. TMAO is directly or indirectly involved in the pathogenesis of CVDs and is an important risk factor affecting the occurrence and even prognosis of CVDs. This review presents the biological and chemical characteristics of TMAO, and the process of TMAO produced by gut microbiota. In particular, the review focuses on summarizing how the increase of gut microbial metabolite TMAO affects CVDs including atherosclerosis, heart failure, hypertension, arrhythmia, coronary artery disease, and other CVD-related diseases. Understanding the mechanism of how increases in TMAO promotes CVDs will potentially facilitate the identification and development of targeted therapy for CVDs.

Subsequent maternal sleep deprivation aggravates neurobehavioral abnormalities, inflammation, and synaptic function in adult male mice exposed to prenatal inflammation.

Objective: Studies have suggested that prenatal exposure to inflammation increases the risk of neuropsychiatric disorders, including anxiety, depression, and cognitive dysfunction. Because of anatomical and hormonal alterations, pregnant women frequently experience sleep dysfunction, which can enhance the inflammatory response. The aim of this study was to explore the effects of maternal sleep deprivation on prenatal inflammation exposure-induced behavioral phenotypes in offspring and identify the associated mechanisms. Methods: Pregnant mice received an intraperitoneal injection of lipopolysaccharide (LPS) on gestational day 15 and were subsequently subjected to sleep deprivation during gestational days 15-21. Anxiety-like behavior was evaluated by the open field test and the elevated plus maze test. Depression-like behavior was assessed by the tail suspension test and the forced swimming test. Cognitive function was determined using the Morris water maze test. The levels of markers of inflammation and synaptic function were examined employing general molecular biological techniques. Results: The results showed that prenatal exposure to LPS resulted in anxiety- and depression-like symptoms and learning and memory deficits, and these effects were exacerbated by maternal sleep deprivation. Furthermore, maternal sleep deprivation aggravated the prenatal LPS exposure-induced increase in the expression of interleukin (IL)-1ß, IL-6, and tumor necrosis factor-α and decrease in the levels of postsynaptic density-95 and synaptophysin in the hippocampus. Discussion: Collectively, these results suggested that maternal sleep deprivation exacerbates anxiety, depression, and cognitive impairment induced by prenatal LPS exposure, effects that were associated with an inflammatory response and synaptic dysfunction.

Melatonin improves the removal and the reduction of Cr(VI) and alleviates the chromium toxicity by antioxidative machinery in Rhodobacter sphaeroides.

Bioremediation with photosynthetic bacteria (PSB) is thought to be a promising removal method for hexavalent chromium [Cr(VI)]-containing wastewater. In the present study, Rhodobacter sphaeroides (R. sphaeroides) SC01 was used for the investigation of Cr(VI) removal in Cr(VI)-contaminated solution in the presence of melatonin. It was found that exogenous melatonin alleviated oxidative damage to R. sphaeroides SC01, increased Cr (VI) absorption capacity of cell membrane, and improved the reduction efficiency of Cr(VI) via the activation of chromate reductants. The results showed that melatonin could further promote the increase in Cr(VI) removal efficiency, reaching up to 97.8%. Furthermore, melatonin application resulted in 296.9%, 44.4%, and 69.7% upregulation of ascorbic acid (AsA), glutathione (GSH), and cysteine (Cys) relative to non-melatioin treated R. sphaeroides SC01 at 48 h. In addition, the resting cells, cell-free supernatants (CFS), and cell-free extracts (CFE) with melatonin had a higher Cr(VI) removal rate of 18.6%, 82.0%, and 15.2% compared with non-melatonin treated R. sphaeroides SC01. Fourier transform infrared spectroscopy (FTIR) revealed that melatonin increased the binding of Cr(III) with PO43- and CO groups on cell membrane of R. sphaeroides SC01. X-ray diffractometer (XRD) analysis demonstrated that melatonin remarkably bioprecipitated the production of CrPO4·6H2O in R. sphaeroides SC01. Hence, these results indicated that melatonin plays the important role in the reduction and uptake of Cr(VI), demonstrating it is a great promising strategy for the management of Cr(VI) contaminated wastewater in photosynthetic bacteria.

Resveratrol ameliorates maternal immune activation-associated cognitive impairment in adult male offspring by relieving inflammation and improving synaptic dysfunction.

Maternal exposure to inflammation may represent a major risk factor for neuropsychiatric disorders with associated cognitive dysfunction in offspring in later life. Growing evidence has suggested that resveratrol exerts a beneficial effect on cognitive impairment via its anti-inflammatory and antioxidant properties and by ameliorating synaptic dysfunction. However, how resveratrol affects maternal immune activation-induced cognitive dysfunction and the underlying mechanisms are unclear. In the present study, pregnant dams were given an intraperitoneal injection of lipopolysaccharide (LPS; 50 µg/kg) on gestational day 15. Subsequently, the offspring mice were treated or not with resveratrol (40 mg/kg) from postnatal day (PND) 60 to PND 88. Male offspring were selected for the evaluation of cognitive function using the Morris water maze test. The hippocampal levels of pro-inflammatory cytokines were examined by ELISA. The mRNA and protein levels of sirtuin-1 (SIRT1), brain-derived neurotrophic factor (BDNF), postsynaptic density protein 95 (PSD-95), and synaptophysin (SYP) were determined by RT-qPCR and western blot, respectively. The results showed that male offspring mice exposed to LPS in utero exhibited learning and memory impairment. Additionally, the levels of interleukin (IL)-1ß, IL-6, and tumor necrosis factor-alpha (TNF-α) were increased while those of SIRT1, BDNF, PSD-95, and SYP were decreased in male offspring of LPS-treated mothers. Treatment with resveratrol reversed cognitive impairment and attenuated the increase in the levels of pro-inflammatory cytokines induced by maternal immune activation in the offspring mice. Furthermore, resveratrol reversed the deleterious effects of maternal immune activation on SIRT1, BDNF, PSD-95, and SYP levels in the hippocampus. Collectively, our results suggested that resveratrol can effectively improve learning and memory impairment induced by maternal immune activation via the modulation of inflammation and synaptic dysfunction.

A highly conductive self-assembled multilayer graphene nanosheet film for electronic tattoos in the applications of human electrophysiology and strain sensing.

Highly conductive, conformable and gel-free electrodes are desirable in human electrophysiology. Besides, intimately coupling with human skin, wearable strain sensors can detect numerous physiological signals, such as wrist pulse and breath. In this study, a multilayer graphene nanosheet film (MGNF) with high conductivity was prepared by the Marangoni self-assembly for using in tattoo dry electrodes (TDEs) and in a graphene tattoo strain sensor (GTSS). Compared to commercial Ag/AgCl gel electrodes, TDEs have lower skin-electrode contact impedance and could detect human electrocardiogram for 24-hour wearing more accurately as well as electromyogram. Through designing a slim serpentine ribbon structure, a resistance-type GTSS, without deterioration even after 2000 cycles, is well demonstrated for human wrist pulse and breath sensing. With the advantages of high conductivity and conformability, MGNF provides support to fabricate low-cost, customizable, and high-performance electronic tattoos for human electrophysiology and strain sensing.

[Suppressive effect of gypenosides on murine leukemia L1210 cell lines].

OBJECTIVE: To investigate the suppressive effect of gypenosides (Gyp) on murine leukemia L1210 cells. METHODS: The growth inhabitation of murine leukemia L1210 cell was detected by MT assay. The production of reactive oxygen species and the change of mitochondrial membrane potential were detected by flow cytometry. The change of nuclear and DNA damage of murine leukemia L1210 cells were detected by DAPI staining and single cell gel electrophoresis. RESULTS: Gyp (100-500 microg/mL) inhibited the growth of murine leukemia L1210 cells. The concentration of Gyp (350 microg/mL) treated murine leukemia L1210 cells at different time points, the mitochondrial membrane potential decrease obviously. L1210 cells were treated with Gyp (350 microg/mL) for 4 h, the highest production of reactive oxygen species was induced. DNA damage were detected after Gyp (350 microg/mL) treated for 4, 12, 24 h. The change of nuclear was treated by Gyp (350 microg/mL) with time-dependent. CONCLUSION: Gypenosides has effects on cell viability, induce reactive oxygen species and decreases mitochondrial membrane potential, and can induce morphological changes and DNA damage.

Anti-inflammatory effects of Rhodiola rosea L.: A review.

Rhodiola rosea L., a worldwide botanical adaptogen, has been confirmed to possess protective effects of inflammatory injury for many diseases, including cardiovascular diseases, neurodegenerative diseases, diabetes, sepsis, and cancer. This paper is to review the recent clinical and experimental researches about the anti-inflammatory effects and the related mechanisms of Rhodiola rosea L. extracts, preparations, and the active compounds. From the collected information reviewed, this paper will provide the theoretical basis for its clinical application, and provide the evidences or guidance for future studies and medicinal exploitations of Rhodiola rosea L.

Baicalein attenuates pancreatic inflammatory injury through regulating MAPK, STAT 3 and NF-κB activation.

Acute pancreatitis (AP) is a common acute abdominal disease with local or systemic inflammatory response, caused by abnormal activation of digestive enzymes. Baicalein has been shown to exert anti-inflammatory effects and to attenuate the pathological changes of AP. The aim of the research was to investigate the effects of baicalein on caerulein induced pancreatitis, and to elucidate the putative underlying mechanism. In this study, the therapeutic potential of baicalein and its mechanism were investigated in a caerulein-induced AP in vivo and in vitro model. The results indicate that baicalein treatment alleviates the caerulein-induced pathological damage in the pancreas. Baicalein decreased the expression level of pro-inflammatory cytokines and chemokines of the pancreas in caerulein treated mice and of isolated pancreatic acinar cells. Moreover, baicalein inhibited the expression of NF-κB p65 and the phosphorylation of p38 MAPK, ERK (extracellular signal-regulated kinase) as well as STAT 3, which indicates that baicalein exerts its anti-inflammatory effects via dampening the NF-κB, MAPK and STAT 3 signaling pathways. Together, this study provides experimental evidence for the clinical application of Scutellaria baicalensis Georgi or baicalein and indicates that baicalein may be a promising candidate for treatment of AP patients in the future.

Gamma Oscillation Dysfunction in mPFC Leads to Social Deficits in Neuroligin 3 R451C Knockin Mice.

Neuroligins (NLs) are critical for synapse formation and function. NL3 R451C is an autism-associated mutation. NL3 R451C knockin (KI) mice exhibit autistic behavioral abnormalities, including social novelty deficits. However, neither the brain regions involved in social novelty nor the underlying mechanisms are clearly understood. Here, we found decreased excitability of fast-spiking interneurons and dysfunction of gamma oscillation in the medial prefrontal cortex (mPFC), which contributed to the social novelty deficit in the KI mice. Neuronal firing rates and phase-coding abnormalities were also detected in the KI mice during social interactions. Interestingly, optogenetic stimulation of parvalbumin interneurons in the mPFC at 40 Hz nested at 8 Hz positively modulated the social behaviors of mice and rescued the social novelty deficit in the KI mice. Our findings suggest that gamma oscillation dysfunction in the mPFC leads to social deficits in autism, and manipulating mPFC PV interneurons may reverse the deficits in adulthood.

[Expression and Clinical Significance of N-cadherin in Bone Marrow Leukemic Cells Derived from Patients with Acute Leukemia].

OBJECTIVE: To investigate the expression of N-cadherin in bone marrow leukemic cells derived from acute leukemia patients and its clinical significances. METHODS: A total of 113 patients with acute leukemia were enrolled in this study. Flow cytometry was employed to detect the expression of N-Cadherin in bone marrow leukemic cells from acute leukemia patients and the relationships between the N-cadherin expression and the clinical characteristics of patients with acute leukemia were analyzed. RESULTS: The expression of N-Cadherin in bone marrow leukemic cells deriveted from patients with acute leukemia was variable with 0%-99.7%. For adult AML patients, the positive rate of CD34 in N-cadherin+ group was significantly higher than that in N-cadherin- group(67.39% vs 33.33%)(P=0.013), while the differences of total CR rate and rate of CR after 1 cycle of induction treatment were not significant between these 2 groups(P>0.05). As to ALL patients, N-cadherin+ group had significant lower WBC count (21.31±7.07 vs 51.10±23.69)(P=0.008) and lower percentage of peripheral blood blast (43.22±5.75% vs 66.45±5.65%)(P=0.015). The CR rate after 1 cycle of induction treatment and rate of overall CR were lower and the relapse rate was higher in N-cadherin+ ALL group than those in N-cadherin- ALL group, but the differences were not significant (P>0.05). For childhood ALL, the positive rate of CD33 in N-cadherin+ group was significantly higher than that in N-cadherin- group(47.62% vs 0%)(P=0.012). The relapse rate was higher in N-cadherin+ group than that in N-cadherin- group (30.00% vs 0%)(P=0.115). The median survival time, 3-year overall OS rate and 3-year relapse-free survival rate in N-cadherin- groups of adult AML, non-M3 AML, ALL and chidhood ALL paients were superior to N-cadherin+ groups, but the differences were not significant. CONCLUSION: The expression of N-cadherin in bone marrow leukemic cells relates to some clinical features of patients with acute leukemia and to some extent has inferior effect on survival of patients with acute leukemia.

[Peripheral blood lymphocyte subsets and their relation with early response to treatment in patients with low or intermediate risk myelodysplastic syndrome (IPSS score ≤ 1.0) and chronic aplastic anemia].

The purpose of this study was retrospectively to analyze the peripheral blood lymphocyte subset distribution in patients with low or intermediate risk myelodysplastic syndromes (IPSS ≤ 1.0) and chronic aplastic anemia (CAA), and their hematological changes of peripheral blood after treatment, so as to understand differences and their relation with early treatment response. The lymphocyte subsets in peripheral blood of 67 patient with low or intermediate risk MDS (IPSS ≤ 1.0), 54 patients with CAA and 73 healthy individuals were analyzed by flow cytometry. The results showed that Th cells, Th/Ts ratio in peripheral blood of low or intermediate risk MDS were 42.94% ± 10.80% and 1.80% ± 0.99% respectively, and were significantly higher than those in control group; the CD16(+) CD56(+) cell ratio was 11.22% ± 7.97%, and was significantly lower than that in control group, the difference was statistically significant (P < 0.05); Ts cells and CD19(+) cell ratio in peripheral blood of CAA patients were 30.87% ± 9.11% and 16.98% ± 7.40% respectively, and were significantly higher than those in control group; CD16(+) CD56(+) cell ratio was 9.81% ± 7.00%, and was significantly lower than that in normal control group, and the difference was statistically significant (P < 0.05); while the Th cells and Th/Ts ratio in low or intermediate risk MDS group were significantly higher than those in CAA group, and the difference was statistically significant (P < 0.05). After treatment for 6 mouths, the HI-E and HI-N rates in CD19(+) cell normal group of low or intermediate risk MDS patients were 18.2% (4/22) and 13.6% (3/22), and were significantly lower than that in the increased group and decreased group. In Ts cell increased group HI-N rate was 15.4% (2/13), and was significantly lower than that in normal group and decreased group. In Th/Ts ratio decreased group HI-N rate was 14.3% (2/14), and was significantly lower than that in the increase group and normal group, the difference was statistically significant (P < 0.05). After treatment of CAA for 6 months, the effective rate for CD3(+) cells, Th cells, Th/Ts ratio in decreased group was 71.4% (5/7), 56.3% (9/16), 50.0% (10/20), and were significantly higher than those in increased and normal group, and the difference was statistically significant (P < 0.05). It is concluded that the peripheral blood lymphocyte subsets of low or intermediate risk MDS(IPSS score ≤ 1.0) and CAA are abnormal, and these lymphocyte subsets are related with hematologic changes after early response to treatment.