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The present study was designed to test the hypothesis that butylphthalide protects the brain of Alzheimer's disease (AD) model rats by inhibiting apoptosis. Ninety Sprague-Dawley rats were randomly divided into drug, control and blank groups of 30 rats in each. The rats in the drug and control groups were treated to induce AD. Then, the rats in the drug group were administered with butylphthalide daily, the rats in the AD control group were given normal saline, and the rats in the healthy group were fed routinely. All rats were sacrificed after 30 days; the brain tissues were used for testing for apoptosis by the terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling (TUNEL) staining method, for determining mitogen-activated protein kinase (MAPK), ERK and P21 protein by western blot analysis, and their cognate mRNA levels by RT-PCR. The results of the TUNEL staining indicated that apoptosis of the brain tissues of rats in the drug group was significantly less than that in the control group and blank group. The protein expression levels of MAPK in the drug group were significantly lower than that in the control group, but higher than that in the normal healthy group (P<0.05). The mRNA expression levels of MAPK in the drug group were significantly lower than those in the control group, but higher than those in the normal healthy group (P<0.05). Based on these results, butylphthalide showed a protective apoptosis-inhibition effect on the brain tissues of the AD rats and this seems to be a consequence of its inhibition of the expressions of MAPK mRNA and MAPK protein in the brain of the rat. [ABSTRACT FROM AUTHOR]

Acute superior mesenteric venous thrombosis (ASMVT) is an intractable disease with poor prognosis. Argatroban, a direct thrombin inhibitor, may be a novel anticoagulant method in the therapy of ASMVT. The aim of the present study was to assess the efficacy and safety of early argatroban therapy in ASMVT patients. The current retrospective study reviewed a consecutive series of ASMVT patients receiving early argatroban therapy during hospitalization between March 2013 and April 2014, with 18 ASMVT patients included in the study. Of these, 16 patients without hepatic dysfunction underwent anticoagulant therapy with argatroban with a mean dose of 1.57±0.34 µg/kg/min and a mean duration of 12.2±3.7 days, while their activated partial thromboplastin time (aPTT) was elevated to 1.95±0.26 times the baseline value. In addition, 2 hepatic dysfunction patients received therapy with a dose of 0.41 µg/kg/min and 0.46 µg/kg/min, and with aPTT of 1.68 and 1.62 times the baseline value, respectively. Overall, 94% (n=17) of the patients presented clinical improvement, while 88% (n=16) of patients presented partially or completely dissolved thrombus in contrast-enhanced computed tomography images. The incidence of surgery and bowel resection was 6% (excluding 1 case with intestinal necrosis detected on admission). Furthermore, 11% (n=2) of patients experienced a bleeding episode, however no major bleeding or mortality occurred during hospitalization. During the follow-up, the mortality and the recurrence rate were 6% and 11%, respectively. In conclusion, early initiation of argatroban treatment may be an effective and safe therapy in ASMVT, manifesting efficient resolution of the thrombus, rapid improvement of symptoms, low incidence of bowel resection and bleeding complication, and low mortality rate. [ABSTRACT FROM AUTHOR]

The aim of the present study was to analyze the mechanism by which nerve growth factor (NGF) promotes callus formation in mice with tibial fracture. NGF transgenic homozygotic mice and NGF wild homozygotic mice were selected to construct non-stabilized fracture model of tibia. The mice were sacrificed on days 7, 14 and 21, respectively, and each group had a sample with 8 mice at each point in time. X-ray radiography and safranin fast green were used to observe fracture healing and in situ hybridization was used to examine the NGF mRNA expression of tibia at each phase of fracture healing. Tartrate-resistant acid phosphatase (TRAP) staining of callus tissue and the expression level of TRAP mRNA were combined to observe osteoclast formation. COL2A1, a chondrocyte differentiation-related gene in callus, and the mRNA level of SOX9 were combined to observe chondrocyte differentiation. It was found that under X-ray radiography, the fracture of NGF transgenic homozygotic mice healed in advance (P<0.05). Cartilage and bone tissue were identified by safranin and fast green staining. The residual cartilage on the callus tissue of NGF transgenic homozygotic mice had decreased significantly (P<0.05). The NGF mRNA expression level in each phase of callus formation of NGF transgenic homozygotic mice was significantly higher than that of the wild group (P<0.05). The number of positive cells in NGF-TRAP staining at each time point after fracture and the NGF mRNA expression level was markedly higher than that of the wild group, and the expression levels of COL2A1 and SOX9 mRNA were distinctively higher than that of the wild group. In conclusion, NGF potentially improves the healing of tibial fracture by osteoclast formation. Additionally, an increase in the number of osteoblasts in the NGF transgenic homozygotic mice compared with the wild-type mice may be achieved by cartilage differentiation due to NGF increasing the COL2A1 and SOX9 mRNA expression levels. [ABSTRACT FROM AUTHOR]

Extracellular matrix metalloproteinase inducer (EMMPRIN) reportedly has a key regulatory role in matrix metalloproteinase (MMP) activities and the progression of atherosclerosis. Statins, which are anti-atherosclerotic pharmacological agents, are widely applied in clinical settings. The aim of the present study was to investigate the pharmaceutical effect of atorvastatin on EMMPRIN expression in atherosclerotic plaques. An atherosclerotic mouse model was established using apoliprotein E-deficient (ApoE-/-) mice raised on a high-fat diet. Additionally, a low (5 mg/kg/day) or high dosage (10 mg/kg/day) of atorvastatin suspension was administered orally for eight weeks, beginning on week 7 or 11 respectively. The effects of atorvastatin on atherosclerotic plaque formation and EMMPRIN expression were subsequently determined. The THP-1 cell line was used to investigate the effect of atorvastatin on EMMPRIN expression in vitro. The results demonstrated that the high-fat diet led to vulnerable plaques (VPs) and increased EMMPRIN expression in VPs in ApoE-/- mice. Atorvastatin treatment decreased EMMPRIN expression in the aortas and plaques of ApoE-/- mice. In vitro, oxidized low-density lipoprotein (ox-LDL) induced the expression of cyclooxygenase-2 (COX-2) and EMMPRIN in THP-1 macrophages, and atorvastatin inhibited ox-LDL-induced expression of PGE2, EMMPRIN and COX-2 in THP-1 macrophages. Therefore, the present data indicated that atorvastatin treatment reduces the vulnerability of atherosclerotic plaques and expression of EMMPRIN, and that the inhibitory effect of atorvastatin on EMMPRIN may occur via the COX-2/PGE2 signaling pathway in macrophages. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the correlation between vascular characteristics under narrow band imaging (NBI) and the expression of angiogenic factors of colorectal carcinoma and adenoma, and to evaluate the feasibility of NBI in vivo visualizing angiogenesis. Patients with colorectal polyps, which were pathologically confirmed as early carcinoma and adenoma, were recruited and examined by NBI. The vascular pattern was classified into type I (invisible or faintly visible vasculature), type II (clearly visible microvasculature that is regularly arranged in a round, oval honeycomb-like pattern) and type III (clearly visible microvasculature that is irregularly arranged in size and caliber or has irregular winding). Immunohistochemical staining was performed by cluster of differentiation (CD)34, insulin-like growth factor (IGF)-1 and signal transducer and activator of transcription 3 (STAT3). The histological results were compared with the vascular pattern under NBI. Overall, 64 sites (15 adenocarcinomas, 29 adenomas and 20 normal) from 58 patients were recruited in the study and examined by NBI. A higher proportion of adenomas (82.1%, 23/28) and adenocarcinomas (66.7%, 10/15) had vascular patterns II and III, respectively. The expression of microvessel density (MVD)-CD34 and IGF-1 in normal mucosa compared with adenomas and adenocarcinomas was significantly different (P<0.0001 and P=0.0062, respectively). MVD-CD34, IGF-1 and STAT3 expression in the sites displayed with vascular patterns I, II, and III was different significantly (P<0.0001, P=0.0010 and P=0.0055, respectively). The spearman correlation coefficient between NBI vascular pattern and MVD-CD34, IGF-1 and STAT3 expression was 0.67, 0.41 and 0.40, respectively. In conclusion, vascular-pattern analysis and the use of an NBI system may be a promising tool for evaluating angiogenesis of colorectal lesions in real-time endoscopy. [ABSTRACT FROM AUTHOR]

Due to the safety, convenience and efficacy of subcutaneous administration of bortezomib (scBor), it is becoming increasingly common to treat multiple myeloma (MM) using this treatment method. The current retrospective study suggested a lower incidence of peripheral neuropathy (PN) outcomes and superior efficacy following treatment with scBor combined with thalidomide and dexamethasone (VTD) in MM when compared with intravenous Bor (ivBor) treatment. The data of 81 patients from the Affiliated Hospital of Nantong University between September 2011 and February 2014 were analyzed, including 37 scBor and 44 ivBor patients administered a median (range) of 5.5 (3-8) and 6 (3-10) chemotherapy cycles, respectively. Adverse events (AEs) were assessed according to the National Cancer Institute (NCI) Common Terminology Criteria for AEs, and response and progression were assessed by the International Myeloma Working Group criteria. Evidence of histopathology using transmission electron microscopy (TEM) was obtained from an in vivo model of adult Sprague Dawley (SD) rats. Following bortezomib-based VTD chemotherapy, patients had achieved very good partial remission or demonstrated no significant difference between the scBor and ivBor treatment groups (75.6 vs. 84.1%, respectively; P=0.350). The 1-year progression-free survival (83.8 vs. 84.1%, scBor vs. ivBor; P=0.921) and 1-year overall survival (OS) (91.9 vs. 90.9%, respectively; P=0.926) were also similar. PN rates of all the NCI grades were 51.3 and 61.3% (P=0.371); grade ≥2, 35.1 and 56.8% (P=0.052); and grade ≥3, 32.7 and 20.5% (P=0.015) in the subcutaneous and intravenous treatment groups, respectively, which suggests that severe PN may be less common following scBor treatment. There were no severe injection site reactions in the scBor-treated group. The incidence of adverse events were comparable between the two groups, including thrombocytopenia, anemia, fatigue and gastrointestinal symptoms such as nausea and vomiting. Furthermore, TEM images of the SD rat sciatic nerves revealed that all rats suffered PN to varying degrees, except the control group, and that the PN of ivBor-treated rats (in the presence and the absence of thalidomide) was more severe than that of scBor-treated rats. It was concluded that a subcutaneous dose of bortezomib of 1.3 mg/\m2 may result in a lower incidence and severity of PN, with equivalent efficacy, as a component of combination VTD chemotherapy. [ABSTRACT FROM AUTHOR]

The expression level and prognosis of Toll-like receptor 2 (TLR2) mRNA in peripheral blood mono-nuclear cells of patients with severe sepsis after applying pulse high-volume hemofiltration (PHVHF) were investigated. Sustained PHVHF treatment was carried out on 40 patients on the basis of conventional treatment for up to 72 h. Acute physiology and chronic health evaluation (APACHE) II scores of patients were compared before and after the treatment. CD4+, CD8+ lymphocyte counts and ratios in the peripheral blood were detected using FASort before and 24 and 48 h of PHVHF treatment. Enzyme-linked immunosorbent assay was adopted to detect tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) concentrations in plasma at different time points before and after 24, 48 and 72 h of treatment, while semi-quantitative reverse transcription-polymerase chain reaction technology was used to test TLR2 mRNA expression. After PHVHF treatment, APACHE II, Sequential Organ Failure Assessment scores were decreased (P<0.05). After 72 h of PHVHF treat-ment, TNF-α, IL-10, TLR2 mRNA expression levels in the plasma of patients were significantly decreased compared to before treatment (P<0.05), and the IL-10 / TNF-α ratio was much higher than before treatment (p<0.05). In conclusion, PHVHF can restore the pro-inflammatory/anti-inflammatory balance of the body, thereby improving the overall condition of the patients by removing inflammatory mediators and lowering TLR2 expression of mononuclear cell surface in peripheral blood. [ABSTRACT FROM AUTHOR]

The healing of burn wounds has been widely characterized to be highly intricate, involving processes such as neo-vascularization, granulation, re-epithelialization, inflammation and wound contraction. Various therapies are available for the management of burn wounds; however, a truly effective therapeutic strategy has yet to be identified due to safety issues. The aim of the present study was to assess and confirm the burn wound healing properties of the compounds asiaticoside (AE) and madecassoside (MA), which are found in the herb Centella asiatica. The cytotoxic nature of the AE and MA were inspected and were confirmed to be non-toxic up to 500 ppm. The compounds AE and MA increased monocyte chemoattractant protein-1 production, but caused no significant effect on vascular endothelial growth factor production. In addition, an in vivo animal burn model was employed to represent the features of burn wound healing. Hence, the present results warrant the further investigation of C. asiatica extracts for use in burn healing. [ABSTRACT FROM AUTHOR]

A 38-year-old Chinese man was admitted to the Second Xiangya Hospital of the Central South University (Changsha, China) with heavy proteinuria and rapidly progressing renal failure with nephrotic syndrome. An initial renal biopsy identified collapsing glomerulopathy (CG) with characteristic segmental collapse of the glomerular tuft and marked hypertrophy and hyperplasia of the visceral epithelial cells. A second renal biopsy showed dilation of glomerular capillary loops as a result of effective treatment with rapamycin and anti-viral therapy. Serology for the coxsackie virus antibody was positive when the collapsing lesion was present, and became negative following treatment, which indicated a strong association between the development of CG and coxsackie virus infection. To the best of our knowledge, this is the first case report of CG associated with coxsackie virus infection. [ABSTRACT FROM AUTHOR]

Gynostemma pentaphyllum is a traditional Chinese medicine reported to possess a wide range of health benefits. As the major component of G. pentaphyllum, gypenoside (GP) displays various anti-inflammatory and anti-oxidant properties. However, it is unclear whether GP can protect against ischemia/reperfusion (I/R)-induced renal injury, and the underlying molecular mechanisms associated with this process remain unknown. In the present study, a renal I/R injury model in C57BL/6 mice was established. It was observed that, following I/R, serum concentrations of creatinine (Cr) and blood urea nitrogen (BUN) were significantly increased (P<0.01), indicating renal injury. Pretreatment with GP (50 mg/kg) significantly inhibited I/R-induced upregulation of serum Cr and BUN (P<0.01). Furthermore, renal malondialdehyde levels were significantly reduced in the I/R+GP group, compared with the I/R group (P<0.01), whereas renal tissue superoxide dismutase activity was significantly higher in the I/R+GP group compared with the I/R group (P<0.01). Further investigation demonstrated that pretreatment with GP produced inhibitory effects on the I/R-induced production of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor-α and interferon-γ (P<0.01). In addition, heme oxygenase 1 (HO-1) expression levels were significantly increased in the I/R group compared with the control (P<0.01), indicating the presence of oxidative damage. However, the I/R-induced upregulation of HO-1 was significantly attenuated by pretreatment with GP (P<0.01), which also suppressed I/R-induced apoptosis by inhibiting pro-apoptotic Bax and upregulating anti-apoptotic Bcl-2 in renal cells (P<0.01). Finally, the activity of ERK signaling was significantly increased in the I/R+GP group compared with the I/R group (P<0.05), which may be associated with the protective effect of GP against I/R-induced renal cell apoptosis. To conclude, the present results suggest that GP produces a protective effect against I/R-induced renal injury as a result of its anti-inflammatory and anti-apoptotic properties. [ABSTRACT FROM AUTHOR]

Melanogenesis is a physiological process that results in the synthesis of melanin pigments, which serve a crucial function in hyperpigmentation. The aim of the present study was to determine the effects of angiotensin II (Ang II) on melanogenesis and to elucidate the molecular events of Ang II-induced melanogenesis. Experiments were performed on human melanocytes to elucidate the pigmenting effect of Ang II and the underlying mechanisms. The elements involved in melanogenesis, including melanin content, tyrosinase (TYR) activity, and microphthalmia-associated transcription factor (MITF) and TYR expression at the mRNA and protein levels were evaluated. Melanin content and TYR activity increased in response to Ang II treatment in a concentration-dependent manner. MITF and TYR mRNA and protein expression levels were increased significantly in response to Ang II in a concentration-dependent manner. The Ang II-induced increase in melanin synthesis was reduced significantly in response to co-treatment with Ro-32-0432, a protein kinase C (PKC) inhibitor, whereas co-treatment with H-89, a PKA inhibitor, did not attenuate the Ang II-induced increase in melanin levels. These results suggest that PKC is required for Ang II-induced pigmentation in human melanocytes and that the mechanism involves the PKC pathway and MITF upregulation. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the effect of the traditional Chinese medicine (TCM), 'Spleen-kidney-care' Yiqi Huayu and Jiangzhuo decoction (SKC-YJ), as an adjuvant therapy in diabetic nephropathy (DN) treatment. In total, 72 patients with DN were randomly divided into control (n=54) and experimental (n=18) groups, with the latter administered SKC-YJ treatment. Indicators for determining the condition of the patients included the levels of proteinuria, blood glucose, glycosylated hemoglobin, blood lipids, blood viscosity and C-reactive protein, which were used to analyze the treatment protocols for DN. Following SKC-YJ treatment, the urinary albumin excretion rate, fasting blood glucose, 2 h-postprandial blood glucose, glycosylated hemoglobin, triglyceride, total cholesterol, blood viscosity, fibrinogen and C-reactive protein levels were detected in the two groups, and were all demonstrated to decrease significantly following treatment with SKC-YJ. Furthermore, the results revealed that SKC-YJ treatment exhibited no significant side-effects on the blood, liver and renal functions or gastrointestinal reactions. By contrast, SKC-YJ improved the symptoms of nausea, vomiting and diarrhea in the patients with DN, while showing no allergic reaction during the observation period. Therefore, SKC-YJ treatment was shown to significantly improve the clinical efficacy of DN treatment, illustrating novel roles for TCM in DN treatment. [ABSTRACT FROM AUTHOR]

This study aimed to observe the expression of dynamin-related protein-1 (Drp-1) in the renal interstitium in a rat model of renal interstitial fibrosis induced by unilateral ureteral obstruction (UUO). In addition, the renoprotective effect of erythropoietin in this model was investigated. A total of 81 rats were randomly assigned to sham surgery, UUO model and treatment groups. Following surgery, the rats in the treatment group were subcutaneously administered erythropoietin at a dose of 3,000 IU/kg once a week until the time of sacrifice. Rats in the sham surgery and UUO model groups were administered an identical volume of normal saline. In each group, nine rats were chosen randomly for sacrifice on days 7, 14 and 21 after surgery for histological examination of renal tissue. Renal tissue specimens were examined by hematoxylin and eosin and Masson's trichrome staining. Immunohistochemical analysis was performed to determine the expression of Drp-1 in the renal interstitium. Renal function damage, as evaluated by the measurement of serum creatinine (Cr) and blood urea nitrogen (BUN) levels, was less severe in the treatment group compared with that in the model group at day 21 (P<0.01). Compared with the UUO model group, the renal interstitial injury score and fibrotic area of the treatment group were decreased markedly at the three time points (P<0.05). The expression level of Drp-1 in the treatment group was decreased markedly at the three time points compared with that in the model group (P<0.05). In conclusion, the expression of Drp-1 is increased in rat renal interstitial fibrosis, and erythropoietin may alleviate the degree of renal interstitial fibrosis by downregulating the expression of Drp-1. [ABSTRACT FROM AUTHOR]

Liver dysfunction reflects the status of heart failure, and previous studies have demonstrated that serum lactate dehydrogenase (S-LDH) levels are increased in patients exhibiting heart failure and liver dysfunction. Right heart failure is a main characteristic of idiopathic pulmonary arterial hypertension (IPAH). The aim of the present study was to assess the prognostic significance of S-LDH levels in patients with IPAH. S-LDH levels were determined in 173 patients with IPAH, and these patients were subclassified into two groups according to a defined upper reference limit of S-LDH (250 IU/l). Right heart catheterization was performed in all patients. A total of 53 patients were found to have elevated S-LDH to ≥250 IU/l. In a mean follow-up period of 31.2±17.9 months, 57 patients succumbed. In the group with lower S-LDH levels (S-LDH <250 IU/l), 16.7% of the patients succumbed, compared with 69.8% of patients in the group with higher S-LDH levels (S-LDH ≥250 IU/l). The Kaplan-Meier survival curves demonstrated that patients with higher S-LDH levels had a significantly lower survival rate than did those with lower S-LDH levels (log-rank test, P<0.001). Cox proportional hazard analyses identified reduced body mass index, reduced cardiac index, elevated World Health Organization functional class, higher S-LDH and an absence of PAH-targeted therapy as significant predictors of adverse outcomes. In conclusion, elevated S-LDH is a risk factor for mortality in patients with IPAH. [ABSTRACT FROM AUTHOR]

Oxidative stress, characterized by increased reactive oxygen species production and/or decreased antioxidant enzyme activity, plays an important role in the pathogenesis of hypertension. The identification of molecular markers corresponding to the oxidative stress status of hypertension may assist in the antioxidant therapy of hypertension. In the present study, superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS) were analyzed as markers of hypertension responding to oxidative stress. The plasma SOD activity and mononitrogen oxides (NOx) concentration were measured, and the SOD3 Ala58Thr and eNOS Glu298Asp polymorphisms were genotyped in hypertensive patients and normotensive controls. Further association experiments were replicated in an extended population, including 343 hypertensive patients and 290 controls. The results demonstrated that no statistically significant differences in the total SOD activity and NOx concentration were identified between the hypertensive patients and controls. However, the plasma SOD activity levels in the SOD3 Ala/Ala homozygote carriers (80.51±27.68 U/ml) were significantly lower compared with the Thr allele carriers (92.18±16.37 U/ml; P=0.031). In addition, the plasma NOx concentration in the eNOS Glu/Glu homozygote carriers (129.66±59.15 µmol/l) was significantly lower compared with the Asp allele carriers (169.84± 55.18 µmol/l; P=0.010). Notably, the altered SOD activity levels and NOx concentration were in concordance in 56.3% of the 80 participants. Therefore, the concordance of decreased SOD activity and NOx concentration, combined with genotypes of SOD3 Ala/Ala and/or eNOS Glu/Glu in hypertensive patients, may be useful in directing the antioxidant therapy of hypertension. [ABSTRACT FROM AUTHOR]

Ischemia-reperfusion (I/R) often leads to acute kidney injury, chronic renal failure and kidney transplantation failure. Glycyrrhizin is extracted from Glycyrrhiza glabra roots and is the predominant active component, which exhibits anti-inflammatory effects. However, to the best of our knowledge, the effect of glycyrrhizin on I/R-induced renal injury has not been investigated. In the present study, glycyrrhizin was demonstrated to attenuate renal I/R injury in mice via administration of glycyrrhizin, which suppressed the serum levels of creatinine and blood urea nitrogen 6 h following reperfusion; furthermore, the superoxide anions as well as the activity of superoxide dismutase within renal tissues was reduced by glycyrrhizin pretreatment. Moreover, the protein level of cleaved caspase-3, as well as its activity in renal tissue, was suppressed as a result of the glycyrrhizin pretreatment, indicating that glycyrrhizin inhibits I/R-induced renal cell apoptosis. In addition, glycyrrhizin pretreatment appeared to ameliorate I/R-induced renal injury via inhibition of inflammatory cell infiltration, as well as the production of pro-inflammatory cytokines, including tumor necrosis factor-α, interferon-γ, interleukin (IL)-1β and IL-6. The underlying molecular mechanism was investigated and it was shown that the activity of p38 mitogen-activated protein kinase signaling was downregulated as a result of glycyrrhizin administration. In conclusion, the present study indicated that glycyrrhizin provided significant protection against I/R-induced renal injury in mice by inhibiting inflammatory responses and renal cell apoptosis. Therefore, glycyrrhizin may be used in abdominal surgery and kidney transplantation for the prevention of renal I/R damage. [ABSTRACT FROM AUTHOR]

In the present study, a case of disseminated abscesses caused by Nocardia in a patient undergoing immunosuppressive therapy for nephrotic syndrome and infected with human immunodeficiency virus (HIV) is described. To the best of our knowledge, this is the first such case to be reported. The patient had membranous nephropathy and received systemic corticosteroid therapy for one year. During this time, the patient was diagnosed with HIV and developed disseminated abscesses in the lungs, brain and hip. Pathogens isolated from sputum and pus were identified as Nocardia asteroides. The patient was successfully treated following surgical drainage of the abscesses and by oral administration of trimethoprim.sulfamethoxazole. [ABSTRACT FROM AUTHOR]

Oxidative stress, characterized by increased reactive oxygen species production and/or decreased antioxidant enzyme activity, plays an important role in the pathogenesis of hypertension. The identification of molecular markers corresponding to the oxidative stress status of hypertension may assist in the antioxidant therapy of hypertension. In the present study, superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS) were analyzed as markers of hypertension responding to oxidative stress. The plasma SOD activity and mononitrogen oxides (NOx) concentration were measured, and the SOD3 Ala58Thr and eNOS Glu298Asp polymorphisms were genotyped in hypertensive patients and normotensive controls. Further association experiments were replicated in an extended population, including 343 hypertensive patients and 290 controls. The results demonstrated that no statistically significant differences in the total SOD activity and NOx concentration were identified between the hypertensive patients and controls. However, the plasma SOD activity levels in the SOD3 Ala/Ala homozygote carriers (80.51±27.68 U/ml) were significantly lower compared with the Thr allele carriers (92.18±16.37 U/ml; P=0.031). In addition, the plasma NOx concentration in the eNOS Glu/Glu homozygote carriers (129.66±59.15 µmol/l) was significantly lower compared with the Asp allele carriers (169.84± 55.18 µmol/l; P=0.010). Notably, the altered SOD activity levels and NOx concentration were in concordance in 56.3% of the 80 participants. Therefore, the concordance of decreased SOD activity and NOx concentration, combined with genotypes of SOD3 Ala/Ala and/or eNOS Glu/Glu in hypertensive patients, may be useful in directing the antioxidant therapy of hypertension. [ABSTRACT FROM AUTHOR]