Clinical outcomes of robotic-assisted and manual total hip arthroplasty in the same patient: A case report.

BACKGROUND: Total hip arthroplasty (THA) is an effective treatment for advanced osteonecrosis of the femoral head, which can significantly relieve pain and improve patients' quality of life. Robotic-assisted THA enhances the accuracy and stability of THA surgery and achieves better clinical outcomes than manual THA. CASE SUMMARY: We report the clinical outcomes of robotic-assisted THA and manual THA in the same patient with osteonecrosis of the femoral head. A 49-year-old male patient attended our hospital due to more than 3 years of pain in both hip joints. The left hip was treated with robotic-assisted THA. The patient underwent manual THA of the right hip 3 mo after robotic-assisted THA. We obtained postoperative radiograph parameters, Harris hip score and forgotten joint score of the patient 1 year after surgery. CONCLUSION: Compared with manual THA, the patient's left hip felt better 1 year after robotic-assisted THA. Robotic-assisted THA resulted in a better Harris hip score and forgotten joint score than manual THA in the same patient with osteonecrosis of the femoral head.

Naringin provides neuroprotection in CCL2-induced cognition impairment by attenuating neuronal apoptosis in the hippocampus.

BACKGROUND: Chemokine C-C motif ligand 2 (CCL2) is one of the most widely recognised proinflammatory chemokines in cognitive disorders. Currently, CCL2-targeting drugs are extremely limited. Thus, this study aimed to explore the neuroprotection afforded by naringin in CCL2-induced cognitive impairment in rats. METHODS: Before the CCL2 intra-hippocampal injection, rats were treated with naringin for 3 consecutive days via intraperitoneal injection. Two days post-surgery, the Morris water maze (MWM) and novel object recognition (NORT) tests were performed to detect spatial learning and memory and object cognition, respectively. Nissl staining and dUTP nick-end labelling (TUNEL) staining were performed to assess histopathological changes in the hippocampus. Commercial kits were used to measure the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine the relative mRNA expression of interleukin 1ß, (IL-1ß), interleukin 6 (IL-6), glutamate/aspartate transporter (GLAST), glutamate transporter-1 (GLT-1), phosphate-activated glutaminase (PAG), cysteine aspartic acid-specific protease 8 (caspase-8), cysteine aspartic acid-specific protease 3 (caspase-3), cell lymphoma/leukaemia-2 (Bcl-2), and Bcl-2 associated X protein (Bax). RESULTS: In the MWM, the average escape latency and average swimming distance were significantly reduced and the crossing times were increased in the naringin-treated groups, compared with the CCL2 group. The NORT results revealed that, compared with the CCL2 rats, the discrimination index in the naringin-treated rats increased significantly. Nissl and TUNEL staining revealed that naringin protected the structure and survival of the neurons in the CA1 zone of the hippocampus. In the naringin-treated groups, the SOD and GSH-Px activities were increased, whereas the MDA levels were decreased. Furthermore, in the naringin-treated groups, the relative mRNA expression of IL-1ß and IL-6 was significantly decreased; GLAST and GLT-1 mRNA expression levels were increased, whereas PAG was decreased. In the naringin-treated groups, the relative mRNA expression levels of caspase-8, caspase-3, and Bax were decreased, whereas that of Bcl-2 was increased. CONCLUSION: Collectively, these data indicated that naringin alleviated the CCL2-induced cognitive impairment. The underlying mechanisms could be associated with the inhibition of neuroinflammation, oxidative stress, apoptosis, and the regulation of glutamate metabolism.

The pedicle screw-rod system is an acceptable method of reconstructive surgery after resection of sacroiliac joint tumours.

UNLABELLED: Hemipelvic resections for primary bone tumours require reconstruction to restore weight bearing along anatomic axes. However, reconstruction of the pelvic arch remains a major surgical challenge because of the high rate of associated complications. We used the pedicle screw-rod system to reconstruct the pelvis, and the purpose of this investigation was to assess the oncology, functional outcome and complication rate following this procedure. The purpose of this study was to investigate the operative indications and technique of the pedicle screw-rod system in reconstruction of the stability of the sacroiliac joint after resection of sacroiliac joint tumours. The average MSTS (Musculoskeletal Tumour Society) score was 26.5 at either three months after surgery or at the latest follow-up. Seven patients had surgery-related complications, including wound dehiscence in one, infection in two, local necrosis in four (including infection in two), sciatic nerve palsy in one and pubic symphysis subluxation in one. There was no screw loosening or deep vein thrombosis occurring in this series. Using a pedicle screw-rod after resection of a sacroiliac joint tumour is an acceptable method of pelvic reconstruction because of its reduced risk of complications and satisfactory functional outcome, as well as its feasibility of reconstruction for type IV pelvis tumour resection without elaborate preoperative customisation. LEVEL OF EVIDENCE: Level IV, therapeutic study.

TMV mutants with poly(A) tracts of different lengths demonstrate structural variations in 3'UTR affecting viral RNAs accumulation and symptom expression.

The upstream pseudoknots domain (UPD) of Tobacco mosaic virus (TMV) is located at the 3'-untranslated region (UTR). It plays an important role in virus replication and translation. To determine the importance of UPD and 3'-UTR, and the effects of introduced RNA elements in TMV 3'-UTR, a series of TMV mutants with internal poly(A) tract upstream of UPD was constructed for structural analysis by selective 2'-hydroxyl acylation analyzed by primer extension (SHAPE). TMV(24A+UPD) and TMV(42A+UPD) formed a similar structure as that of TMV 3'-UTR, but TMV(62A+UPD) structures altered by the introduced poly(A) tract. In addition, TMV(24A+UPD) had a higher viral RNAs accumulation than TMV in N. benthamiana protoplasts, and induced lethal symptoms in the infected plants. TMV(62A+UPD) showed a drastically reduced accumulation, its coat protein was undetectable in protoplasts, and the inoculated plants remained symptomless. This study analyzed the structures of 3'-UTR of TMV and found that the longer poly(A) tract introduced upstream of UPD reduced viral RNAs accumulation and induced milder symptoms in N. benthamiana. In conclusion, different lengths of the internal poly(A) tract introduced into the TMV 3'UTR lead to structural variations that affect virus accumulation and symptom expression.

Increased NOD1, but not NOD2, activity in subcutaneous adipose tissue from patients with metabolic syndrome.

OBJECTIVE: Nucleotide-binding oligomerization domain (NOD) protein, as cytoplasmic receptor of the innate immune response, plays an important role in adipose inflammation and insulin resistance in obesity. Our objective was to examine adipose tissue (AT) NOD in nascent metabolic syndrome (MetS) patients and to investigate its association with MetS features. METHODS: Thirty-four MetS subjects and 31 controls were recruited. Fasting blood was collected, and abdominal subcutaneous AT was obtained by biopsy for NOD1/NOD2 expression and activity. RESULTS: MetS subjects showed significantly increased expression for NOD1 on adipose depots as compared to controls. In addition to increased expression of downstream signaling mediators RIPK2 and NF-κB p65 nuclear translocation, there was remarkably higher release of monocyte chemotactic protein1 (MCP-1), interleukin (IL)-6, and IL-8 in MetS versus controls following priming of the isolated adipocytes with NOD1 ligand iE-DAP. With regard to NOD2, the differences between the two groups were not significant in either basal state or after activation. Increased NOD1 positively correlated with waist circumference. NOD1 was also correlated with HbA1c and HOMA-IR. NOD1 positively correlated with serum levels of IL-6, MCP-1, and NF-κB activity. CONCLUSIONS: Activation of the innate immune pathway via NOD1 may be partially responsible for the increased systemic inflammation and insulin resistance in MetS.

[Study on effects of Tripterygium wilfordii polycoride in resisting macrophage inflammation and regulating inflammation via TLR4/NF-κB].

To investigate the effect of Tripterygium wilfordii polycoride (TWP) on LPS-induced macrophage inflammatory response, particularly the inhibitory effect on inflammatory factors TNF-α and IL-1ß and the regulatory effect on inflammation via TLR4/NF-κB. The MTT method was adopted to test the effects of tested drugs, TWP, dexamethasone (DXM) and azathioprine (AZA) on cell growth to define the appropriate concentration. LPS was used to induce the inflammatory reaction in mouse RAW264. 7 cell lines. The Elisa kit was adopted to test the release level of TNF-α and IL-1ß. The Western blotting was applied to test the protein expressions of TNF-α and IL-1ß. The RT-PCR was adopted to test the expressions of TLR4 and NF-κB. According to the results, TWP could inhibit the release of macrophage inflammatory factors TNF-α and IL-1ß in a dose dependent manner. All of TWP groups showed a weaker efficacy than that of the DXM group. But the TWP high dose group revealed a better effect on TNF-α and equal effect on IL-1ß compared with the AZA group. TWP show an equal or better effect in down-regulating TLR4 and NF-κB p65 expressions in a dose dependent manner than DXM and AZA. In conclusion, TWP could inhibit TLR4 and NF-κB p65, which may be related to the down-regulation of TLR4 and NF-κB p65 receptor expressions.

[Effect of carbon disulfide on mitochondrial apoptosis-related proteins in cytoplasm of testicular tissue among male rats].

OBJECTIVE: To investigate the role of mitochondrial pathway in the apoptosis of spermatogenic cells induced by inhalation of carbon disulfide in male rats. METHODS: Twenty-four male Sprague-Dawley rats (clean grade) were divided into four groups according to their body weights: three CS(2) exposure groups (CS(2) concentrations: 50, 250, and 1250 mg/m(3)) and a control group. The rats in CS(2) exposure groups were exposed to CS(2) by static inhalation for 10 weeks (2 h/d, 5 d/w), while the rats in control group were exposed to air. Then, all rats were sacrificed by decapitation; testicular tissues were collected, and cytoplasmic proteins were extracted; the levels of apoptosis-inducing factor (AIF), cytochrome c (cyto c), Bcl-2, Bax, procaspase-9, and procaspase-3 were measured by Western blot, and the activities of caspase-9 and caspase-3 were measured using a test kit. RESULTS: Compared with the control group, all CS(2) exposure groups had significantly increased levels of cyto c in the cytoplasm of testicular tissue (P<0.05); in the 250 mg/m(3) CS(2) exposure group, the Bax/Bcl-2 ratio and activities of caspase-9 and caspase-3 increased significantly (P<0.05), and the content of procaspase-9 and procaspase-3 decreased significantly (P<0.05); in the 1250 mg/m(3) CS(2) exposure group, the relative expression levels of Bax and AIF in cytoplasm increased significantly (P<0.05), and the expression level of Bcl-2 decreased significantly (P<0.05). CONCLUSION: Mitochondrial pathway plays an important role in the CS(2)-induced apoptosis of spermatogenic cells in testicular tissue among male rats.

[Analysis of associations between molecular subtypes and responses to neoadjuvant chemotherapy in primary breast cancer patients].

OBJECTIVE: To explore the correlations between molecular subtypes and responses to neoadjuvant chemotherapy in primary breast cancer patients. METHODS: The core-needle biopsy specimens were collected from 563 patients undergoing 4-8 cycles of neoadjuvant chemotherapy between January 2001 to January 2009. And immunohistochemical assays were employed to detect the levels of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and Ki-67 proliferation index simultaneously. Molecular subtypes were divided on the basis of immunohistochemical results. And the associations between molecular subtypes and responses to neoadjuvant chemotherapy were analyzed in 563 patients. RESULTS: The pathological complete response (pCR) rates of patients with hormone receptor-negative/HER2-negative subtype (HR-/HER2-) , HER2-positive subtype (HER2+) and hormone receptor-positive/HER2-negative subtype (HR+/HER2-) were 38.9%, 17.9% and 8.3% respectively. In univariate analysis, there were significant differences in pCR rates among the groups (P < 0.001) . In multivariate analysis, the patients with HER2+ subtype had a significantly higher pCR rate than those with HR+/HER2- subtype (OR = 0.344, P = 0.002) . Whereas the patients with HER2+ subtype had a significantly lower pCR rate than those with HR-/HER2- subtype (OR = 2.453, P = 0.007) . Among HR+/HER2-subtypes, a higher pCR rate was observed in the group of high expression level of Ki-67 proliferation index (Ki-67 ≥ 20%) (P = 0.004) . But no significant differences existed in pCR rates between the group of high expression level of hormone receptor and the group of non-high expression level (P = 0.256) . CONCLUSION: There were correlations between molecular subtypes and responses to neoadjuvant chemotherapy in primary breast cancer patients. Patients of HER2+and HR-/HER2- subtype are more likely to respond to neoadjuvant chemotherapy. Among HR+/HER2-subtypes, those with a high level of Ki-67 proliferation index tend to benefit from neoadjuvant chemotherapy.

Saturated fatty acid induces insulin resistance partially through nucleotide-binding oligomerization domain 1 signaling pathway in adipocytes.

OBJECTIVE: To investigate the potential role of nucleotide-binding oligomerization domain 1 (NOD1), a component of the innate immune system, in mediating lipid-induced insulin resistance in adipocytes. METHODS: Adipocytes from Toll-like receptor 4 deficiency mice were used for stimulation experiments. The effect of oleate/palmitate mixture on nuclear factor-κB (NF-κB) activation was analyzed by reporter plasmid assay. The release of proinflammatory chemokine/cytokines production was determined by using real-time PCR. Insulin-stimulated glucose uptake was measured by 2-deoxy-D-[3H] glucose uptake assay. Chemokine/cytokine expression and glucose uptake in adipocytes transfected with small interfering RNA (siRNA) targeting NOD1 upon fatty acids treatment were analyzed. RESULTS: Oleate/palmitate mixture activated the NF-κB pathway and induced interleukin-6, tumor necrosis factor-α, and monocyte chemoattractant protein-1 mRNA expressions in adipocytes from mice deficient in Toll-like receptor 4, and these effects were blocked by siRNA targeting NOD1. Furthermore, saturated fatty acids decreased the ability of insulin-stimulated glucose uptake. Importantly, siRNA targeting NOD1 partially reversed saturated fatty acid-induced suppression of insulin-induced glucose uptake. CONCLUSION: NOD1 might play an important role in saturated fatty acid-induced insulin resistance in adipocytes, suggesting a mechanism by which reduced NOD1 activity confers beneficial effects on insulin action.

Active lipids of Ganoderma lucidum spores-induced apoptosis in human leukemia THP-1 cells via MAPK and PI3K pathways.

ETHNOPHARMACOLOGICAL RELEVANCE: Ganoderma lucidum (Lingzhi) is traditionally drug, which has been traditionally effective used in the treatment of chronic hepatopathy, hypertension, hyperglycemia and cancer. MATERIALS AND METHODS: THP-1 and HL-60 apoptosis induced by active lipids of Ganoderma lucidum spores was quantified by flow cytometry using FITC-conjugated annexin V and PI; MAPK and Akt were measured by Western blot, and caspase-3, -8 and -9 activities were also detected by spectrophotometric assay. RESULTS: Our results showed that active lipids of Ganoderma lucidum spores decreased phosphorylation-ERK1/2 (P-ERK1/2), P-Akt and increased P-JNK1/2, but did not affect expressions of P-p38 MAPK in THP-1 cells. Moreover, treatment of THP-1 cells with active lipids of Ganoderma lucidum spores resulted in activation of caspase-3, -8 and -9. Furthermore, LY294002 (Akt inhibitor) or PD98059 (ERK1/2 inhibitor) significantly enhanced active lipids of Ganoderma lucidum spores-induced apoptosis in THP-1 cells, whereas caspase inhibitors or SP600125 (JNK inhibitor), decreased apoptosis in THP-1 cells. CONCLUSION: Taken together, our study for the first time suggests that active lipids of Ganoderma lucidum spores is able to enhance apoptosis in THP-1 cells, at least in part, through inhibition of ERK1/2, Akt and activation of JNK1/2 signaling pathways. Moreover, it also triggers caspase-3, -8 and -9 activation mediated apoptotic induction.

Characterization of a wheat heme oxygenase-1 gene and its responses to different abiotic stresses.

In animals and recently in plants, heme oxygenase-1 (HO1) has been found to confer protection against a variety of oxidant-induced cell and tissue injuries. In this study, a wheat (Triticum aestivum) HO1 gene TaHO1 was cloned and sequenced. It encodes a polypeptide of 31.7 kD with a putative N-terminal plastid transit peptide. The amino acid sequence of TaHO1 was found to be 78% similar to that of maize HO1. Phylogenetic analysis revealed that TaHO1 clusters together with the HO1-like sequences in plants. The purified recombinant TaHO1 protein expressed in Escherichia coli was active in the conversion of heme to biliverdin IXa (BV), and showed that the V(max) was 8.8 U·mg(-1) protein with an apparent K(m) value for hemin of 3.04 µM. The optimum Tm and pH were 35 °C and 7.4, respectively. The result of subcellular localization of TaHO1 showed that the putative transit peptide was sufficient for green fluorescent protein (GFP) to localize in chloroplast and implied that TaHO1 gene product is at least localized in the chloroplast. Moreover, we found that TaHO1 mRNA could be differentially induced by the well-known nitric oxide (NO) donor sodium nitroprusside (SNP), gibberellin acid (GA), abscisic acid (ABA), hydrogen peroxide (H(2)O(2)) and NaCl treatments. Therefore, the results suggested that TaHO1 might play an important role in abiotic stress responses.

Jolkinolide B from Euphorbia fischeriana Steud induces apoptosis in human leukemic U937 cells through PI3K/Akt and XIAP pathways.

Jolkinolide B, a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud, is known to induce apoptosis in cancer cells. However, the molecular mechanism of its anti-cancer activity has not been fully elucidated. In the present study, we found that Jolkinolide B reduced cell viability and induced apoptosis in a dose- and time-dependent manner in human leukemic U937. The induction of apoptosis was also accompanied by the downregulation of PI3K/Akt and the inhibitor of apoptosis protein (IAP) family proteins. Moreover, we observed that Jolkinolide B treatment resulted in activation of caspase-3 and -9, which may partly explain the anti-cancer activity of Jolkinolide B. Taken together, our study for the first time suggest that Jolkinolide B is able to enhance apoptosis of U937 cells, at least in part, through downregulation of PI3K/Akt and IAP family proteins. Moreover, triggering of caspase-3 and -9 activation mediated apoptotic induction.

Staphylococcus aureus induces apoptosis of human monocytic U937 cells via NF-kappaB signaling pathways.

Staphylococcus aureus (S. aureus) is an opportunistic pathogen and the major causative agent of numerous infections. S. aureus have been shown to induce apoptosis in many cell types. However, the mechanisms regulating primary monocytes and human monocytic U937 cell death following S. aureus challenge are unknown. In this study, we found that infection of primary monocytes and human monocytic U937 cells with S. aureus induced rapid cell death in a dose- and time-dependent manner displaying the characteristic features of apoptosis. Studying the underlying mechanisms we found that the S. aureus-induced apoptosis was associated with a more prominent reduction in expression of the anti-apoptotic protein nuclear transcription factor-kappaB (NF-kappaB). Because expressions of anti-apoptotic Bcl-2, survivin, inhibition of apoptosis protein (cIAP), and X-chromosome-linked inhibitor of apoptosis protein (XIAP) are regulated by NF-kappaB, S. aureus decreased the levels of these proteins in U937 cells through inhibition of NF-kappaB. Moreover, S. aureus induced apoptotic genes (Bax and caspase-3) expression, and exposure of primary monocytes and U937 cells to S. aureus led to caspase-3 activity. Collectively, these data define a pathway that infection of primary monocytes and U937 cells with S. aureus induces a caspase-dependent inhibition of NF-kappaB.

The role of the lactadherin in promoting intestinal DCs development in vivo and vitro.

Lactadherin, as one of the immune components in the breast milk, might play a role in the intestinal immune system of newborn. Therefore, we investigated the effect of lactadherin-feeding in early time on the development of intestinal immune system compared with naturally rearing and artificially rearing (non-lactadherin). In the present study, we observed that the Peyer's Patches (PP) from the pups of artificially reared group with lactadherin added were characterized by an excess of OX62(+)CD4(+)SIRP(+) DC cells and a higher expression of CD3(+)CD4(+)CD25(+)T cells. Additionally, this study also demonstrated that IL-10 production was dramatically increased when lactadherin was present in culture medium compared with lactadherin-absent culture. These results suggested that lactadherin could adjust intestinal DCs activity, induce CD3(+)CD4(+)CD25(+)T cell differentiation, and enhance IL-10 production.

Hepatocyte growth factor prevents advanced glycation end products-induced injury and oxidative stress through a PI3K/Akt-dependent pathway in human endothelial cells.

AIMS: Advanced glycation end products (AGEs) trigger an oxidative reaction which then accelerates endothelial cell apoptosis; this is a critical event in the process of diabetic vascular complications. We previously demonstrated that hepatocyte growth factor (HGF) protects human endothelial cells against AGE-induced injury. The present study was designed to investigate the possible involvement of MAPK and PI3K/Akt signaling in the action of HGF. MAIN METHODS: HUVECs were treated with AGEs in the presence or absence of HGF. For detection of apoptosis, the morphological Acridine Orange staining, flow cytometry, and caspase-3 activity assay were used. Generation of reactive oxygen species (ROS) and the change in mitochondrial membrane potential were measured using flow cytometry and fluorescence immune analysis. The activation of MAPK and Akt was assayed by Western blot. KEY FINDINGS: HGF exerted its prosurvival effect by inhibiting the overproduction of intracellular ROS and the depolarization of mitochondrial membrane, induced by AGEs. HGF-induced survival correlated with Akt activity and was inhibited by the specific PI3K inhibitor. ERK also was activated by HGF and rescued cells from apoptosis, although the cytoprotective effect was less marked than for PI3K/Akt. HGF-mediated survival was independent of JNK and p38MAPK pathways. Furthermore, blocking the PI3K and Akt activities with PI3K inhibitors or transfection of HUVECs with the dominant-negative p85 or Akt effectively abolished the inhibition of the intracellular ROS production and mitochondrial damage. SIGNIFICANCE: Our studies suggest that HGF, via PI3K/Akt signaling, prevents AGE-induced apoptosis and oxidative stress through the inhibition of mitochondrial damage in HUVECs.

Phosphoinositide 3-kinase/Akt and nuclear factor-kappaB are involved in Staphylococcus aureus-induced apoptosis in U937 cells.

OBJECTIVE: To explore the mechanisms involved in Staphylococcus aureus (S. aureus) invading human monocytic U937 cells. METHODS: S. aureus were added to U937 cells at multiplicity of infections (MOI) of 20:1 for 0, 15, 30, 60, and 90 minutes, respectively. Cell apoptosis was analyzed with Hoechst 33258 staining and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry analysis. Akt and nuclear factor-kappaB (NF-kappaB) activities were detected by Western blotting. RESULTS: Infection of U937 cells with S. aureus induced rapid cell death in a time-dependent manner, and the cells displayed characteristic features of apoptosis. S. aureus-induced apoptosis was associated with a prominent downregulation of activated (phosphorylated) Akt and NF-kappaB. The inhibition of phosphorylated Akt by LY294002 led to the inhibition of NF-kappaB in a dose-dependent manner. Inhibition of Akt with LY294002 caused further increase in apoptosis of U937 cells. CONCLUSIONS: S. aureus can stimulate the apoptosis of U937 cells. S. aureus induces apoptosis of U937 cells by inhibiting Akt-regulated NF-kappaB.

Hepatocyte growth factor protects against apoptosis induced by advanced glycation end products in endothelial cells.

OBJECTIVE: To investigate the effects of hepatocyte growth factor (HGF) on vascular endothelial cells apoptosis induced by advanced glycation end products (AGEs) and its possible mechanism. METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured in vitro and intervened by different concentrations of AGEs and HGF. The cell inhibitory rates of each group with different culture time (12, 24, 48, and 72 hours) were measured by methyl thiazolyl tetrazolium (MTT) assay. The early stage apoptosis was detected by flow cytometry with Annexin V-FITC/PI double staining, morphology of cell apoptosis was observed by hoechst 33258 fluorescence staining, and the expression of apoptosis-associated genes Bax and Bcl-2 were determined by Western blotting. The activity of caspase-3 was detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: Morphological observation indicated that high concentration of AGEs induced characteristic apoptotic changes in HUVECs. Within a certain concentration range, HUVECs apoptosis inducing rates by AGEs were in both dose- and time-dependent manners. HGF significantly inhibited the apoptosis of HUVECs induced by AGEs (P < 0.05). AGEs significantly promoted expression of Bax protein, but not Bcl-2. Whereas HGF significantly promoted the expression of Bcl-2 (P < 0.01) and decreased the activity of caspase-3 (P < 0.05) without affecting Bax level. CONCLUSIONS: AGEs can induce the apoptosis of endothelial cells in vitro. HGF may effectively attenuate AGEs-induced endothelial cells apoptosis through upregulating Bcl-2 gene expression and inhibiting caspase-3 activation.