Platelets, small pieces of cytoplasm with biological activity, split and fall off the megakaryocytes and mature from the bone marrow. After stimulated, platelets produce nitric oxide to inhibit their own activation and aggregation. Pathologically, the injury of endothelial cells activates platelets and changes their functions. The release of inflammatory mediators and cytokines induces and enhances the development and progression of atherosclerosis, and thereby promotes the occurrence of erectile dysfunction. Besides, platelets and their related functional parameters may serve as important indicators in the diagnosis and treatment of erectile dysfunction.
Atherosclerosis ; etiology ; Blood Platelets ; physiology ; Cytokines ; metabolism ; Endothelial Cells ; Erectile Dysfunction ; etiology ; Humans ; Male ; Nitric Oxide ; biosynthesis ; Platelet Activation

This paper aims to investigate the effect of store-operated calcium channels (SOC) and receptor-operated calcium channels (ROC) on Ca(2+)-sensing receptor (CaR)-induced extracellular Ca(2+) influx and nitric oxide (NO) generation in human umbilical vein endothelial cells (HUVEC). SOC blocker, non-selective cation channel blocker, ROC agonist and ROC blocker were used separately and combined. Intracellular Ca(2+) concentration ([Ca(2+)]i) was measured by Fura-2/AM loading. The activity of endothelial nitric oxide synthase (eNOS) and the production of NO were determined by the DAF-FM diacetate (DAF-FM DA). The results showed that increases of [Ca(2+)]i, eNOS activity and NO generation induced by CaR agonist Spermine were all reduced after single blocking the SOC or ROC, respectively (P < 0.05). ROC agonist can partially abolish the ROC blocker's effect (P < 0.05). The above mentioned effects evoked by CaR agonist Spermine were further reduced when blocking both SOC and ROC than single blocking SOC or ROC in HUVEC (P < 0.05). In conclusion, these results suggest that the SOC and ROC participate in the processes of CaR-evoked extracellular Ca(2+) influx and NO generation by a synergistic manner in HUVEC.
Calcium ; physiology ; Calcium Channel Blockers ; pharmacology ; Calcium Channels ; physiology ; Calcium Signaling ; Fluoresceins ; pharmacology ; Human Umbilical Vein Endothelial Cells ; physiology ; Humans ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase Type III ; metabolism ; Receptors, Calcium-Sensing ; physiology

BACKGROUNDPomegranate (punica granatum) belongs to the family Punicaceae, and its peel has been used as a traditional Chinese medicine because of its efficacy in restraining intestine, promoting hemostasis, and killing parasites. Pomegranate peel has been reported to possess wound-healing properties which are mainly attributed to its polyphenol extracts. The purpose of this study was to investigate the effect of pomegranate peel polyphenols (PPP) gel on cutaneous wound healing in diabetic rats.

METHODSAlloxan-induced diabetic rats were given incisional wounds on each side of the mid-back and then treated daily with PPP gel (polyphenol mass fraction = 30%) post-wounding. Rats were sacrificed on days 4, 7, 14, and 21 post-wounding to assess the rates of wound closure, histological characteristics; and to detect the contents of hydroxyproline, production of nitric oxide (NO), and activities of NO synthase (NOS), as well as the expressions of transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF) in wound tissue.

RESULTSWound closure was significantly shortened when PPP gel was applied to the wounds of diabetic rats. Histological examination showed the ability of PPP gel to increase fibroblast infiltration, collagen regeneration, vascularization, and epithelialization in the wound area of diabetic rats. In addition, PPP gel-treated diabetic rats showed increased contents of hydroxyproline, production of NO, and activities of NOS and increased expressions of TGF-β1, VEGF, and EGF in wound tissues.

CONCLUSIONPPP gel may be a beneficial method for treating wound disorders associated with diabetes.

Alloxan ; Animals ; Diabetes Mellitus, Experimental ; pathology ; physiopathology ; Female ; Gels ; Hydroxyproline ; analysis ; Male ; Nitric Oxide ; biosynthesis ; Polyphenols ; pharmacology ; Punicaceae ; Rats ; Rats, Wistar ; Transforming Growth Factor beta1 ; physiology ; Vascular Endothelial Growth Factor A ; physiology ; Wound Healing ; drug effects

Heat shock protein 27 belongs to the heat shock protein family in the small molecular weight family. This review collected a number of literature to analyze the expression meaning and mechanism of HSP27,expounded HSP27 with inhibition of NO production, maintenance of cell protein stability and accelerated cell damage repair function. At the same time, HSP27 also has a resistance to apoptosis, protecting mitochondria, inhibiting activation of nuclear factor and other related functions. The heat shock protein 27 has protection in spinal cord ischemia-reperfusion.
Apoptosis ; HSP27 Heat-Shock Proteins ; physiology ; Humans ; Nitric Oxide ; biosynthesis ; Reperfusion Injury ; prevention & control ; Spinal Cord ; blood supply

The present study is aimed to investigate the effect of chronic intermittent hypobaric hypoxia (CIHH) on contractile activities in isolated thoracic aorta and pulmonary artery rings and the underlying mechanism in rats. Sprague-Dawley (SD) rats were randomly divided into 4 groups: control group (CON), 14 days CIHH treatment group (CIHH14), 28 days CIHH treatment group (CIHH28) and 42 days CIHH treatment group (CIHH42). CIHH rats were exposed to hypoxia in a hypobaric chamber simulating 5 000 m altitude, 6 h daily for 14, 28 and 42 d, respectively. After artery rings were prepared from pulmonary artery and thoracic aorta, the contractile activity of the artery rings was recorded using organ bath technique. Results are shown as follows. (1) There were no significant differences of noradrenaline (NA)- and KCl-induced contractions in thoracic aorta and pulmonary artery rings among CIHH and CON rats. (2) Angiotensin Ⅱ (ANGⅡ)-induced contraction in thoracic aorta rings, not in pulmonary artery rings, of CIHH rats was decreased compared with that in CON rats. There was no significant difference of ANGⅡ-induced contraction in thoracic aorta rings among CIHH rats. (3) Inhibitory effect of CIHH on ANGⅡ-induced contraction in thoracic aorta rings was endothelium-independent, and was reversed by glibenclamide (Gli), an ATP-sensitive potassium channels (K(ATP)) blocker, and L-NAME, a NO synthase inhibitor, but not by indomethacin (Indo), a cyclooxygenase inhibitor. These results suggest that CIHH attenuates the contraction induced by ANGⅡ in thoracic aorta rings of rat, which is related to the opening of K(ATP) channel and the increased production of NO.
Angiotensin II ; pharmacology ; Animals ; Aorta, Thoracic ; physiopathology ; Hypoxia ; physiopathology ; KATP Channels ; metabolism ; Male ; Muscle Contraction ; physiology ; Muscle, Smooth, Vascular ; physiopathology ; Nitric Oxide ; biosynthesis ; Pulmonary Artery ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Vasoconstriction ; physiology

Effect of sodium nitroprusside (SNP), a nitric oxide (NO) donor, on in vitro survival, growth, steroidogenesis, and apoptosis of buffalo preantral follicles (PFs) was investigated. PFs (200~250 microm) were isolated by micro-dissection and cultured in 0 (control), 10(-3), 10(-5), 10(-7), and 10(-9) M SNP. To examine the reversible effect of SNP, PFs were cultured with 10(-5) M SNP + 1 mM Nomega-nitro-L-arginine methyl ester (L-NAME) or 1.0 microg hemoglobin (Hb). The results showed that greater concentrations of SNP (10(-3), 10(-5), 10(-7) M) inhibited (p < 0.05) FSH-induced survival, growth, antrum formation, estradiol production, and oocyte apoptosis in a dose-dependent manner. However, a lower dose of SNP (10(-9) M) significantly stimulated (p < 0.05) the survival, growth, antrum formation, follicular oocyte maturation, and stimulated progesterone secretion compared to the control. A combination of SNP + L-NAME promoted the inhibitor effect of SNP while a SNP + Hb combination reversed this effect. Nitrate and nitrite concentrations in the culture medium increased (p < 0.05) in a dose-dependent manner according to SNP concentration in the culture medium. At higher concentrations, SNP had a cytotoxic effect leading to follicular oocyte apoptosis whereas lower concentrations have stimulatory effects. In conclusion, NO exerts a dual effect on its development of buffalo PFs depending on the concentration in the culture medium.
Animals ; *Apoptosis ; Buffaloes/*physiology ; Estradiol/biosynthesis ; Female ; Follicle Stimulating Hormone/metabolism ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitrates/pharmacology ; Nitric Oxide/*metabolism ; Nitric Oxide Donors/pharmacology ; Nitrites/pharmacology ; Nitroprusside/pharmacology ; Oocytes/cytology/drug effects/growth & development/metabolism ; Ovarian Follicle/*cytology/drug effects/growth & development/*metabolism ; Progesterone/biosynthesis

OBJECTIVE: To determine the effect of pregnancy-associated plasma protein A (PAPP-A) on the function of vascular endothelial cells (VEC). METHODS: Human umbilical vein endothelial cell (HUVEC) line, derived from human umbilical vein, was cultured in vitro with PAPP-A at 0, 50, 100, and 200 ng/mL for 0, 12, 24, and 48 hours, respectively. Nitric oxide (NO) levels and endothlin-1 (ET-1) levels were determined by spectrophotometer and immunehistory. RESULTS: The NO levels of HUVECs in the PAPP-A groups were significantly lower than those in the control group (P<0.05). The ET-1 levels of HUVECs in the PAPP-A groups were significantly higher than those in the control group (P<0.05). The changes were all dose-dependent. CONCLUSION PAPP-A may affect the function of vascular endothelial cells by reducing the secretion of NO and increasing the level of ET-1.
Cell Line ; Endothelial Cells ; cytology ; metabolism ; physiology ; Endothelin-1 ; biosynthesis ; Female ; Humans ; Nitric Oxide ; biosynthesis ; Pregnancy-Associated Plasma Protein-A ; pharmacology ; Umbilical Veins ; cytology ; metabolism

OBJECTIVETo investigate the effects of Shexiang Baoxin Pill (SBP) on function of endothelial progenitor cells (EPCs) and its nitric oxide (NO) secretion.

METHODSTotal mononuclear cells were isolated from human peripheral blood by ficoll density gradient centrifugation and inoculated on the human fibro-ligandin encrusting plate. After 7 days of in vitro culture, adherent cells were collected and incubated with SBP for 24 h. The proliferation, migration, adhesive activity, vasculogenesis capacity and NO secretion of EPCs were assayed using MTT, Transwell chamber, adhesion determination, in vitro vasculogenesis kit and nitrate reductase method, respectively.

RESULTSEPCs incubated with SBP showed the capacities higher than those of control in proliferation, migration, adhesion, in vitro vasculogenesis, and with a higher NO concentration in the culture supernatant.

CONCLUSIONSBP can improve the function of EPCs, which might be a novel mechanism of its effects in improving vascular endothelial function and promoting angiogenesis.

Cell Differentiation ; physiology ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Endothelial Cells ; cytology ; metabolism ; physiology ; Humans ; Leukocytes, Mononuclear ; cytology ; Nitric Oxide ; biosynthesis ; Stem Cells ; cytology ; metabolism ; physiology

The efflux of nitro oxide (NO) in the duration of storing red blood cells (RBCs) was the main reason resulting in decrease and even loss of vasodilatory activity, cell deformability and ability of carrying oxygen (O2) in the stored RBCs. The deep understanding physical functions and acting ways of NO in circulatory system, as well as transformations and balance control of S-Nitrosohemoglobin (SNO-Hb) has an important significance for ensuring sure safety and efficacy of transfusion. In this article, the physical functions, acting ways, retaining and transferring form of nitro oxide, and SNO-Hb adjusting, as well as effects of SNO-Hb concentration on change on stored red blood cells were reviewed.
Erythrocytes ; metabolism ; physiology ; Hemoglobins ; biosynthesis ; Humans ; Nitric Oxide ; metabolism

BACKGROUNDBradykinin (BK) acts mainly on two receptor subtypes: B(1) and B(2), and activation of B(2) receptor mediates the most well-known cardioprotective effects of angiotensin converting enzyme inhibitors (ACEi), however, the role that B(1) receptor plays in ACEi has not been fully defined. We examined the role of B(1) receptor in the inhibitory effect of ACE inhibitor captopril on rat cardiomyocyte hypertrophy and cardiac fibroblast proliferation induced by angiotensin II (Ang II) and explored its possible mechanism.

METHODSNeonatal cardiomyocytes and cardiac fibroblasts (CFs) were randomly treated with Ang II, captopril, B(2) receptor antagonist (HOE-140) and B(1) receptor antagonist (des-Arg(10), Leu(9)-kallidin) alone or in combination. Flow cytometry was used to evaluate cell cycle, size and protein content. Nitric oxide (NO) and intracellular cyclic guanosine monophosphate (cGMP) level were measured by colorimetry and radioimmunoassay.

RESULTSAfter the CFs and cardiomyocytes were incubated with 0.1 micromol/L Ang II for 48 hours, the percentage of CFs in the S stage, cardiomyocytes size and protein content significantly increased (both P < 0.01 vs control), and these increases were inhibited by 10 micromol/L captopril. However, NO and cGMP levels were significantly higher than that with Ang II alone (both P < 0.01). 1 micromol/L HOE-140 or 0.1 micromol/L des-Arg(10), Leu(9)-kallidin attenuated the effects of captopril, which was blunted further by blockade of both B(1) and B(2) receptors.

CONCLUSIONSActing via B(2) receptor, BK contributes to the antihypertrophic and antiproliferative effects of captopril on cardiomyocytes and CFs. In the absence of B(2) receptor, B(1) receptor may act a compensatory mechanism for the B(2) receptor and contribute to the inhibition of cardiomyocyte hypertrophy and CFs proliferation by captopril. NO and cGMP play an important role in the effect of B(1) receptor.

Angiotensin-Converting Enzyme Inhibitors ; pharmacology ; Animals ; Animals, Newborn ; Captopril ; pharmacology ; Cardiomegaly ; prevention & control ; Cell Proliferation ; drug effects ; Cell Size ; drug effects ; Cyclic GMP ; analysis ; DNA ; biosynthesis ; Fibroblasts ; drug effects ; physiology ; Myocytes, Cardiac ; drug effects ; pathology ; Nitric Oxide ; analysis ; Rats ; Rats, Sprague-Dawley ; Receptor, Bradykinin B1 ; physiology