OBJECTIVETo investigate the regulation on endothelial function of sapindus saponins in spontaneously hypertensive rats by studying the reactivity on different vasoconstrictor and dilator, and the content of the active substances.

METHODForty 16-week-old spontaneously hypertensive rats were randomly divided into five groups, one with placebo as model group, one with captopril tablets (27 mg x kg(-1)) as positive control, one with low-dose sapindus saponins (27 mg x kg(-1)), one with medium-dose (54 mg x kg(-1)), one with high-dose (108 mg x kg(-1)). And another eight healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for eight weeks, and the indicators to be detected were as follows: (1) the response of thoracic aorta on different vasoconstrictors Ang II (1 x 10(-9) -1 x 10(-5) mol x L(-1)), PE (1 x 10(-8) 1 x 10(-4) mol x L(-1)), KCl (20 -120 mmol x L(-1)); (2) the endothelium-dependent or non-endothelium-dependent vasodilation response of thoracic aorta on Ach (1 x 10-(10)-1 x 10(-5) mol x L(-1)) or SNP (1 x 10(-8)-1 x 10(-3) mol x (L(-1); (3) the content of NO, 6-KPG1alpha, ET-1 and TXB2 in serum was determined by Elisa.

RESULTIn SHR model group, the response of thoracic aorta on Ang II, PE and KCl was increased, the endothelium-dependent vasodilation on Ach was reduced, but the effects on SNP was not obvious, the content of ET-1 and TXB2 was increased, and the content of NO and 6-KPG1alpha was reduced, Vs the normal control group, there were significant differences (P < 0.05 or P < 0.01); in the treatment groups, the response of thoracic aorta on Ang II, PE and KCl was reduced, the endothelium-dependent vasodilation of thoracic aorta on Ach was improved, the content of ET-1 and TXB2 was reduced, and the content of NO and 6-KPG1alpha was increased, Vs the SHR model group, there were significant differences (P < 0.05 or P < 0.01).

CONCLUSIONOur findings suggested that sapindus saponins protected the endothelial function in SHR, the mechanisms were relevant to the protection of endothelial function.

Angiotensin II ; pharmacology ; Animals ; Aorta, Thoracic ; drug effects ; physiology ; Endothelin-1 ; analysis ; Endothelium, Vascular ; drug effects ; physiology ; Female ; Male ; Nitric Oxide ; analysis ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Sapindus ; chemistry ; Saponins ; pharmacology

AIMTo observe the alterations in the biochemical and biophysical changes in the sperm membrane during sperm maturation in male rats treated with the water extract of the fruit pericarp of S. mukorossi.

METHODSAdult male Sprague-Dawley rats were gavaged the aqueous extract of the fruit pericarp of S. mukorossi at a dose of 50 mg/kg/d for 45 days. On day 46, the sperm parameters were observed in different sections of the epididymis and the sperm superoxide dismutase and the lipid peroxidation was determined and compared with the controls. The testis and epididymis were routinely prepared for histological examination under the light microscope.

RESULTSNo significant differences in the sperm number and morphology were observed between the control and treated groups. However, a significant inhibition (P<0.05-0.01) of sperm motility in the caput, corpus and cauda regions of the epididymis was seen in the treated group. No significant histopathological changes were found in the testis and epididymis. The important finding was that in the treated animals, the spermatozoa showed an abnormal distribution of the superoxide dismutase activity, being minimum in the caput and maximum in the corpus, which was just opposite to that of the controls.

CONCLUSIONThe study provides a unique observation where the plant extract alters the sperm membrane physiology without change the testicular and epididymal morphology.

Animals ; Cell Membrane ; drug effects ; Epididymis ; cytology ; drug effects ; Lipid Peroxidation ; drug effects ; Male ; Malondialdehyde ; metabolism ; Plant Preparations ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Sapindus ; Sperm Maturation ; drug effects ; Spermatozoa ; drug effects ; enzymology ; Superoxide Dismutase ; metabolism

OBJECTIVETo observe the effects of sapindoside on blood pressure, Ang II, Ald, ET in the blood plasma and NO in the serum in renovascular hypertension rat.

METHODThe 2K1C (2 kidney 1 clap) hypertensive model rats were used and drugs had been given by ig. for 5 weeks. The blood pressure was measured at the 1, 3, 7, 14, 21, 28, 35 day after drug. At the end of 5th weeks, the Ang II, Ald, ET in the blood plasma and NO in the serum were measured.

RESULTSapindoside (H, M and L) by ig. for 5 weeks could significantly lower the blood pressure, increase the levels of NO in the serum, reduce the concentration of Ang II, Ald, ET in the blood plasma.

CONCLUSIONSapindoside plays an important role in decreasing the blood pressure of renovascular hypertension rat.

Aldosterone ; blood ; Angiotensin II ; blood ; Animals ; Antihypertensive Agents ; isolation & purification ; pharmacology ; Blood Pressure ; drug effects ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Endothelins ; blood ; Female ; Hypertension, Renovascular ; blood ; physiopathology ; Male ; Nitric Oxide ; blood ; Oleanolic Acid ; analogs & derivatives ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Sapindus ; chemistry ; Saponins ; isolation & purification ; pharmacology

OBJECTIVETo investigate the effects of sapindus saponins on myocardial inflammation mediated by Ang II/ p38MAPK signal pathway and cardiac hypertrophy in spontaneously hypertensive rats. And also to explore the correlation of cardiac hypertrophy and inflammation.

METHODThirty-two 16-week-old spontaneously hypertensive rats (SHR) were randomly divided into four groups, one with placebo as model group, one with captopril tablets (27 mg x kg(-1)) as positive control, one with low-dose sapindus saponins (27 mg x kg(-1)), one with high-dose (108 mg x kg(-1)). And another eight healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for eight weeks, and the indicators detected were as follows: (1) left ventricular mass index (LVMI); (2) the content of Ang II and hs-CRP in plasma were determined by ELISA; (3) the protein expression of AT1R and VEGF were determined by immunohistochemical method; (4) the protein expression of p-p38MAPK in myocardial cells was determined by Western blot.

RESULTSapindus saponins reduced LVMI, and blocked the expression level of Ang II, AT1R, p-p38MAPK, VEGF and hs-CRP in myocardial tissue. Vs the SHR model group, there were significant differences (P < 0.05 or P < 0.01).

CONCLUSIONOur findings suggested that sapindus saponins could inhibited cardiac hypertrophy, the possible mechanisms may be related to the inhibition on inflammatory response mediated by Ang II/p38MAPK pathway.

Angiotensin II ; immunology ; Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Humans ; Hypertension ; complications ; drug therapy ; immunology ; Hypertrophy, Left Ventricular ; drug therapy ; etiology ; immunology ; Male ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Wistar ; Sapindus ; chemistry ; Saponins ; administration & dosage ; p38 Mitogen-Activated Protein Kinases ; immunology

OBJECTIVESTo investigate the protective effects of Sapindus saponins in spontaneously hypertensive rats, and the possible cellular and molecular mechanisms.

METHODSThirty-two 16-week-old spontaneously hypertensive rats were randomly divided into four groups (8 in each group): model group (placebo), positive control group (27 mg/kg of Captopril Tablets), Sapindus saponins groups (27 mg/kg and 108 mg/kg, respectively). Another 8 healthy Wistar-Kyoto strain (WKY) rats were used as the normal group. The animals were treated for 8 weeks. Blood pressure of rats was determined by non-invasive blood pressure meter (BP-6). Furthermore, the contents of angiotensin II (Ang II) in plasma and myocardial tissue were determined by enzyme-linked immunosorbent assay (ELISA), the gene expression of receptor angiotensin type 1 (AT1R) in aorta was determined by quantitative realtime polymerase chain reaction (qRT-PCR). The protein expression of transforming growth factor-β1 (TGF-β1) and AT1R in heart was determined by immunohistochemical staining. The protein expression of p-phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK) was determined by Western blotting. The contents of interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF) in serum were determined by radioimmunoassay. And the histopathological and morphological changes of aorta and heart tissue samples were assessed semi-quantitatively by hematoxylin-eosin (HE) or Masson staining.

RESULTSThirty minutes after single or continuous treatment, systolic blood pressure (SBP) was reduced significantly in Sapindus saponins groups. And the contents of AngII, IL-1, IL-6 and TNF-α in serum, the expression of AT1R mRNA, p-p38MAPK and TGF-β1 were significantly suppressed dose-dependently (P<0.05 or P<0.01). With the Sapindus saponins treatment, compared with those of the model group, the cardiac and aortic pathological changes were ameliorated significantly.

CONCLUSIONSOur findings suggest that Sapindus saponins might have protective effects in spontaneously hypertensive rats, the cellular and molecular mechanisms of which might be relevant to the regulation of inflammatory responses mediated by p-p38MAPK signal pathway based on activated Ang II and AT1R.

Angiotensin II ; metabolism ; Animals ; Aorta ; drug effects ; pathology ; physiopathology ; Blood Pressure ; drug effects ; Collagen ; metabolism ; Female ; Hypertension ; blood ; drug therapy ; enzymology ; physiopathology ; Interleukin-1 ; blood ; Interleukin-6 ; blood ; Male ; Phosphorylation ; drug effects ; Protective Agents ; pharmacology ; therapeutic use ; Rats, Inbred SHR ; Receptor, Angiotensin, Type 1 ; metabolism ; Renin-Angiotensin System ; drug effects ; Sapindus ; chemistry ; Saponins ; pharmacology ; therapeutic use ; Transforming Growth Factor beta1 ; metabolism ; Tumor Necrosis Factor-alpha ; blood ; p38 Mitogen-Activated Protein Kinases ; metabolism