Effects of aqueous leaf extract of Tridax procumbens on contractile activity of corpus cavernosum in N-nitro-L-arginine methyl ester-induced hypertensive male rats

Objective： This study investigated the effects of aqueous leaf extract of Tridax procumbens （ALETP） on con- tractile activity of corpus cavernosum in N-nitro-L-arginine methyl ester （L-NAME）-induced hypertensive male rats. Methods： Twenty normal, adult male rats （130-150 g） were divided into four groups of five rats each. Group I （control） was given normal saline （0.6 mL/kg） and group II was given L-NAME （40 mg/kg） for 6 weeks. Groups Ill and IV also received L-NAME （40 mg/kg） for 6 weeks but were further co-treated with 100 and 200 mg/kg of ALETP, respectively, from week 4 to week 6. All treatments were given orally. Strips of corpus cavernosum from each of the four groups were exposed to increasing concentrations of acetyl~ choline （ACh） and sodium nitroprusside （SNP） （10^-9-10^-5 tool/L） after contraction with phenylephrine （10^-7 mol/L） to test for a dose-response effect, Response to potassium and calcium was also measured after cumulatively adding potassium and calcium （10-50 mmol/L） to potassium- and calcium-free organ chamber. Isometric contractions were recorded through an Ugo Basile data capsule acquisition system. Results： Mean arterial blood pressure was significantly reduced in the ALETP co-treated group compared to the control and L-NAME-only groups （P 〈 0.05）. Cavernosa strips from ALETP co-treated rats exhibited significant inhibition of contraction in response to phenylephrine, potassium chloride, and calcium chlo- ride （P 〈 0.05）. Relaxation in response to Ach and SNP was also significantly impaired in cavernosa strips from the L-NAME-only treated group （P 〈 0.05）, while ALETP co-treated groups showed enhanced per- centage relaxation. Conclusion： ALETP treatment of L-NAME-induced hypertensive rats promotes a relaxant effect on isolated cavernosa strips. ALETP shows potential in correcting erectile dysfunction in hypertension.

Chloroquine Relieves Acute Lung Injury in Rats with Acute Hemorrhagic Necrotizing Pancreatitis

Summary： This study preliminarily investigated the mechanism by which chloroquine （CQ） relieves acute lung injury （ALI） complicated in acute hemorrhagic necrotizing pancreatitis （AHNP）. Sixty male Wistar rats were randomized into sham-operated group （group A, n=10）, AHNP group （group B, n=10）, L-arginine-treated group （group C, n=10）, L-N-nitro-L-arginine methyl ester （NAME）-treated group （group D, n=10）, CQ-treated group （group E, n=10） and CQ＋L-NAME-treated group （group F, n=10）. TLR4 expression was measured by using real time-PCR and Western blotting respectively. The results showed that, in the group B, the expression of TLR4 and the levels of TNF-α and IL-6 in the lungs were significantly increased, and the nitric oxide （NO） concentration was reduced, as compared with those in the group A （P〈0.05 or P〈0.01）. Lung injury was aggravated with the increased expression of TLR4. When the inhibitor and stimulator of TLR4, namely L-Arg and L-NAME, were added respectively, lung injury was correspondingly relieved or aggravated （P〈0.05 or P〈0.01）. In the group E, TLR4 expres- sion was substantially lower and NO concentration higher than those in the group B （P〈0.05 or P〈0.01）. However, in the group F, NO concentration was markedly decreased, and the inhibitory effect of CQ on TLR4 expression and the relief of lung injury were weakened when compared with those in the group E （P〈0.05 or P〈0.01）. It was concluded that TLR4 may play an important role in the pathogenesis and development of ALl complicated in AHNP. CQ could relieve ALl by decreasing the TLR4 expression and increasing the NO release.

THE ROLE OF NITRIC OXIDE IN SMALL INTESTINAL MIGRATING MOTOR COMPLEX

The main objective is to study the role or nitric oxide (NO) in small Intestinal migratingmotor complex (MMC). Rats were implanted with strain gauges in the duobenum and jejunum forrecording the motor action of the small intestine in fasting and red states arter intravenous infusionof N'-nitro-L-arginine methyl ester (L-NAME ), L-arginin., D-arglnine, sodium nitropusside(NaNP) and angiotensin 1 respectively. The results showed that intravenous inrusion or L-NAME,a NO synthase inhibitor, induced a fasting-like MMC motor pattern in fed rats. Infusion of NaNP, aNO donor, disrupted small intestinal MMC in fasting rats, inducing a postprandial-like motor pattern. Both fasting and postprandial, infusion of L-NAME shortened the duration or Phase I andphase Ⅱ,but didn't chang. the duration, frequency, amplitude and s,eed or Propogatiou of thephaSe, Ⅲ-argining, not D-arginine infused together with L-NAME, prevented the effect of LNAME infusion. Infusion of L-arginine, D-arginine or angioteusin Ⅰ alone didn't modify the smallintestinal motor pattern. It suggests that an inhibition of NO synthesis may be involved in the initiation of the MMC motor pattern during fasting, whereas an increase of NO output relates to the occurrence of the fed motor pattern

Role of nitric oxide in biological effects of vascular endothelial growth factor

To evaluate the role of nitric oxide in the biological effects of vascular endothelial growth factor(VEGF)and the possible mechanism of VEGF,the in vitro cultured vascular endothelial cells of rabbit aorta were divided into control group,VEGF-treated group and VEGF+N-nitro-L-arginine methyl ester(L-NAME)-treated group.The absorbance(A)value of vascular endothelial cells and the levels of prostaglandin(PGI2),endothelin-1(ET-1)and von Willebrand factor(vWF)in the supernatant were observed by water-soluble tetrazo-lium salt assay,radioimmunoassay and enzyme-linked immunosorbent assay.The A values and PGI2 in VEGF-treated group and VEGF+L-NAME-treated group were higher than those in control group(P<0.05 and P<0.01).The ET-1 and vWF were significantly decreased in VEGF-treated group and VEGF+L-NAME-treated group com-pared with the control(P<0.05 and P<0.01).These results indicate that VEGF could promote the proliferation and secretion of PGI2 and inhibit the secretion of ET-1 and vWF in vascular endothelial cells and that L-NAME could inhibit the effect of VEGF partially.Nitric oxide is an important mediator in the process of stimulating prolifera-tion and regulating secretion of vascular endothelial cells by VEGF.