Effects of zinc and manganese on advanced glycation end products (AGEs) formation and AGEs-mediated endothelial cell dysfunction.

AIMS: The present study investigated the effects of ZnCl2 and MnCl2 supplementations on advanced glycation end products (AGEs) formation and AGEs-mediated endothelial cell dysfunction. MAIN METHODS: Fluorescence detection was used to monitor the Maillard reaction. Inductively coupled plasma optical emission spectroscopy was used to test cellular zinc and manganese levels. Real-time reverse transcription polymerase chain reaction and western blot were used to analyze the expression of endothelial nitric oxide synthase (eNOS), nuclear transcription factor kappa B (NF-κB), and receptor for AGEs (RAGE). Intracellular reactive oxygen species (ROS) and nitric oxide (NO) production, NOS activity were determined by fluorescent probe assay, superoxide dismutase (SOD) activity was determined by water soluble tetrazolium salt assay. KEY FINDINGS: MnCl2 showed excellent inhibitory effect on AGEs formation. Primary cultured bovine aortic endothelial cells (BAECs) were exposed to AGEs for 30 min, followed by trace element treatments. Cell viability and the zinc levels declined due to AGEs exposure, which were improved with the supplementations of ZnCl2 and MnCl2. Furthermore, ZnCl2 supplementation effectively enhanced intracellular NO production, elevated eNOS expression and enzymatic activity, and down-regulated NF-κB activation and RAGE expression. MnCl2 dose-dependently impaired ROS formation, down-regulated NF-κB protein expression and nuclear translocation, as well as restored Mn-SOD enzymatic capability. SIGNIFICANCE: Our findings suggested that trace elements relevant to diabetic, such as zinc and manganese played different roles in the formation of AGEs. Both the elements benefited the AGEs-injured BAECs through different mechanisms.

The aqueous extract of Asparagus officinalis L. by-product exerts hypoglycaemic activity in streptozotocin-induced diabetic rats.

BACKGROUND: The inedible bottom part of asparagus (Asparagus officinalis L.) spears, around one-third to one-half of the total length, is always discarded as by-product. Since it still contains various bioactive substances, this by-product might have potential usage in food supplements for its therapeutic effects. In this study the hypoglycaemic effect of the aqueous extract of asparagus by-product (AEA) was evaluated in a streptozotocin (STZ)-induced diabetic rat model. RESULTS: Continuous administration of AEA for 21 days significantly decreased fasting serum glucose and triglyceride levels but markedly increased body weight and hepatic glycogen level in diabetic rats. In an oral glucose tolerance test, both the blood glucose level measured at 30, 60 and 120 min after glucose loading and the area under the glucose curve showed a significant decrease after AEA treatment. CONCLUSION: The results of this study demonstrate that AEA has hypoglycaemic and hypotriglyceridaemic functions, suggesting that it might be useful in preventing diabetic complications associated with hyperglycaemia and hyperlipidaemia.

Hypolipidaemic and hypoglycaemic effects of total flavonoids from seed residues of Hippophae rhamnoides L. in mice fed a high-fat diet.

BACKGROUND: The present study was designed to investigate the hypolipidaemic and hypoglycaemic effects of total flavonoids from seed residues of Hippophae rhamnoides L. (FSH) in a high-fat diet fed mouse model. Consumption of a high-fat diet (HFD) for 4 weeks caused a significant rise of serum total cholesterol in mice. These hypercholesterolaemic mice then were orally administrated with different doses of FSH (50, 100 and 150 mg kg⁻¹ body weight) and simvastatin (20 mg kg⁻¹ body weight) for another 12 weeks under continuous HFD feeding. RESULTS: FSH administration markedly reduced total mouse body, liver, and epididymal fat pad weights. Serum total cholesterol and low density of lipoprotein-cholesterol levels were also significantly decreased by FSH treatment. Additionally, FSH significantly lowered total cholesterol and triglyceride concentrations in liver, and the results were corroborated by transmission electron microscope findings. The rise in serum glucose was significantly suppressed by FSH treatment while improving impaired glucose tolerance. CONCLUSION: These results suggest that FSH possesses hypolipidaemic and hypoglycaemic properties in mice fed a high-fat diet and could be developed as a supplement in healthcare foods and drugs.

(-)-Gossypol suppresses the growth of human prostate cancer xenografts via modulating VEGF signaling-mediated angiogenesis.

(-)-Gossypol, a natural BH3-mimetic and small-molecule Bcl-2 inhibitor, shows promise in ongoing phase II clinical trials for human cancers. However, whether (-)-gossypol plays functional roles in tumor angiogenesis has not been directly elucidated yet. In this study, we showed that (-)-gossypol dose dependently inhibited the expression of VEGF, Bcl-2, and Bcl-xL in human prostate cancer cells (PC-3 and DU 145) and primary cultured human umbilical vascular endothelial cells (HUVEC) in vitro. Notably, the growth of human prostate tumor PC-3 xenografts in mice was significantly suppressed by (-)-gossypol at a dosage of 15 mg/kg/d. This inhibitory action of (-)-gossypol in vivo was largely dependent on suppression of angiogenesis in the solid tumors, where VEGF expression and microvessel density were remarkably decreased. Furthermore, (-)-gossypol inhibited VEGF-induced chemotactic motility and tubulogenesis in HUVECs and human microvascular endothelial cells and suppressed microvessel sprouting from rat aortic rings ex vivo. When examined for the mechanism, we found that (-)-gossypol blocked the activation of VEGF receptor 2 kinase with the half maximal inhibitory concentration of 2.38 µmol/L in endothelial cells. Consequently, the phosphorylation of key intracellular proangiogenic kinases induced by VEGF was all suppressed by the treatment, such as Src family kinase, focal adhesion kinase, extracellular signal-related kinase, and AKT kinase. Taken together, the present study shows that (-)-gossypol potently inhibits human prostate tumor growth through modulating VEGF signaling pathway, which further validates its great potential in clinical practice.

1'-Acetoxychavicol acetate suppresses angiogenesis-mediated human prostate tumor growth by targeting VEGF-mediated Src-FAK-Rho GTPase-signaling pathway.

Cancer therapeutic agents that are safe, effective and affordable are urgently needed. We describe that 1'-acetoxychavicol acetate (ACA), a component of Siamese ginger (Languas galanga), can suppress prostate tumor growth by largely abrogating angiogenesis. ACA suppressed vascular endothelial growth factor (VEGF)-induced proliferation, migration, adhesion and tubulogenesis of primary cultured human umbilical vascular endothelial cells (HUVECs) in a dose-dependent manner. ACA also inhibited VEGF-induced microvessel sprouting from aortic rings ex vivo and suppressed new vasculature formation in Matrigel plugs in vivo. We further demonstrated that the mechanisms of this chavicol were to block the activation of VEGF-mediated Src kinase, focal adhesion kinase (FAK) and Rho family of small guanosine triphosphatases (GTPases) (Rac1 and Cdc42 but not RhoA) in HUVECs. Furthermore, treatment of human prostate cancer cells (PC-3) with ACA resulted in decreased cell viability and suppression of angiogenic factor production by interference with dual Src/FAK kinases. After subcutaneous administration to mice bearing human prostate cancer PC-3 xenografts, ACA (6 mg/kg/day) remarkably inhibited tumor volume and tumor weight and decreased levels of Src, CD31, VEGF and Ki-67. As indicated by immunohistochemistry and TUNEL analysis, microvessel density and cell proliferation were also dramatically suppressed in tumors from ACA-treated mice. Taken together, our findings suggest that ACA targets the Src-FAK-Rho GTPase pathway, leading to the suppression of prostate tumor angiogenesis and growth.

Hypolipidemic effect of n-butanol Extract from Asparagus officinalis L. in mice fed a high-fat diet.

During industrial processing of Asparagus (Asparagus officinalis L.), around half of each spear is discarded. However, these discarded asparagus (by-products) might be used as food supplements for their potential therapeutic effects. This study evaluated the hypolipidemic effect of n-butanol extract (BEA) from asparagus by-products in mice fed a high-fat diet (HFD). Continuous HFD feeding caused hyperlipidemia, oxidative stress and liver damage in mice. Interestingly, while BEA significantly decreased the levels of body weight gain, serum total cholesterol and low density lipoprotein cholesterol, it dramatically increased the high density lipoprotein level when administered at three different doses (40, 80 or 160 mg/kg body weight) for 8 weeks in hyperlipidemic mice. In addition, BEA decreased the levels of alanine transaminase, aspartate transaminase and alkaline phosphatase in serum. Finally, superoxide dismutase activity and the total antioxidation capacity were evidently increased, while the malondialdehyde level and the distribution of lipid droplets were reduced in liver cells of BEA-treated mice. Taken together, the findings of this study suggested that BEA had a strong hypolipidemic function and could be used as a supplement in healthcare foods and drugs or in combination with other hypolipidemic drugs.

Methyl 2-cyano-3,11-dioxo-18-olean-1,12-dien-30-oate (CDODA-Me), a derivative of glycyrrhetinic acid, functions as a potent angiogenesis inhibitor.

Methyl 2-cyano-3,11-dioxo-18-olean-1,12-dien-30-oate (CDODA-Me), a triterpenoid acid derived synthetically from glycyrrhetinic acid, has been characterized as a peroxisome proliferator-activated receptor γ agonist with a broad range of receptor-dependent and -independent anticancer activities. Although CDODA-Me decreases the expression of some angiogenic genes in cancer cells, the direct effects of this compound on angiogenesis have not been defined. In this study, we have extensively investigated the activities of CDODA-Me in multiple angiogenesis assays. Our results showed that this agent inhibited vascular endothelial growth factor (VEGF)-induced proliferation, migration, invasion, and lamellipodium and capillary-like structure formation of human umbilical endothelial cells (HUVECs) in a concentration-dependent manner. Moreover, CDODA-Me abrogated VEGF-induced sprouting of microvessels from rat aortic rings ex vivo and inhibited the generation of new vasculature in the Matrigel plugs in vivo, where CDODA-Me significantly decreased the number of infiltrating von Willebrand factor-positive endothelial cells. To understand the molecular basis of this antiangiogenic activity, we examined the signaling pathways in CDODA-Me-treated HUVECs. Our results showed that CDODA-Me significantly suppressed the activation of VEGF receptor 2 (VEGFR2) and interfered with the mammalian target of rapamycin (mTOR) signaling, including mTOR kinase and its downstream ribosomal S6 kinase (S6K), but had little effect on the activities of extracellular signal-regulated protein kinase and AKT. Taken together, CDODA-Me blocks several key steps of angiogenesis by inhibiting VEGF/VEGFR2 and mTOR/S6K signaling pathways, making the compound a promising agent for the treatment of cancer and angiogenesis-related pathologies.

Hypolipidaemic and hepatoprotective effects of ethanolic and aqueous extracts from Asparagus officinalis L. by-products in mice fed a high-fat diet.

BACKGROUND: Asparagus (Asparagus officinalis L.) by-products, i.e. the parts of the spears discarded during industrial processing, might have potential use as food supplements for their therapeutic effects. In this study the hypolipidaemic and hepatoprotective effects of ethanolic (EEA) and aqueous (AEA) extracts from asparagus by-products were evaluated in mice fed a high-fat diet (HFD). RESULTS: Continuous HFD feeding caused obvious hyperlipidaemia and liver damage in mice. However, both EEA and AEA significantly decreased the levels of body weight gain, serum total cholesterol and serum low-density lipoprotein cholesterol in hyperlipidaemic mice when administered at a daily dose of 200 mg kg(-1) for 8 weeks. Also, serum high-density lipoprotein cholesterol levels were evidently increased in the AEA-treated group. Moreover, both EEA and AEA dramatically decreased the activities of alanine and aspartate transaminases in serum. Finally, superoxide dismutase activity and total antioxidant capacity were increased and malondialdehyde level and the distribution of lipid droplets decreased in liver cells of both EEA- and AEA-treated mice. CONCLUSION: The findings of this study suggest that both EEA and AEA have strong hypolipidaemic and hepatoprotective properties and could be used as supplements in healthcare foods and drugs or in combination with other hypolipidaemic drugs.

Celastrol suppresses angiogenesis-mediated tumor growth through inhibition of AKT/mammalian target of rapamycin pathway.

Understanding the molecular basis and target of traditional medicine is critical for drug development. Celastrol, derived from Trypterygium wilfordii Hook F. ("Thunder of God Vine"), a traditional Chinese medicine plant, has been assigned anticancer activities, but its mechanism is not well understood. Here, we investigated whether Celastrol could inhibit angiogenesis-mediated tumor growth and, if so, through what mechanism. When given s.c. to mice bearing human prostate cancer (PC-3 cell) xenografts, Celastrol (2 mg/kg/d) significantly reduced the volume and the weight of solid tumors and decreased tumor angiogenesis. We found that this agent inhibited vascular endothelial growth factor (VEGF)-induced proliferation, migration, invasion, and capillary-like structure formation by primary cultured human umbilical vascular endothelial cells (HUVEC) in a dose-dependent manner. Furthermore, Celastrol abrogated VEGF-induced sprouting of the vessels from aortic rings and inhibited vascular formation in the Matrigel plug assay in vivo. To understand the molecular mechanism of these activities, we next examined the signaling pathways in treated HUVECs and PC-3 tumor cells. Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K). Additionally, we found that Celastrol inhibited the proliferation of prostate cancer cells and induced apoptosis, and these effects correlated with the extent of inhibition of AKT/mTOR/P70S6K signaling. Taken together, our results suggest that Celastrol targets the AKT/mTOR/P70S6K pathway, which leads to suppression of tumor growth and angiogenesis.

Hypoglycemic effect of aqueous extract of seabuckthorn (Hippophae rhamnoides L.) seed residues in streptozotocin-induced diabetic rats.

An extract of seabuckthorn (Hippophae rhamnoides L.) seed residues has been shown to possess hypoglycemic and hypolipidemic properties in normal mice. The present study investigated the effects of an aqueous extract of seabuckthorn seed residues (ASSR) on serum glucose, lipid profiles and antioxidant parameters in streptozotocin-induced diabetic rats. Male Sprague-Dawley rats were divided into four groups: a normal control group; diabetic control group; diabetic groups supplemented with 5 mg/kg body weight glibenclamide (reference drug) and 400 mg/kg body weight ASSR. Diabetes in rats was induced by intraperitoneal injection of streptozotocin (45 mg/kg body weight). Vehicle (distilled water), glibenclamide and ASSR were administered orally to normal and diabetic rats once a day lasting for 4 weeks. The data showed that administration of ASSR significantly lowered the serum glucose, triglyceride and nitric oxide levels in diabetic rats. Moreover, ASSR treatment also increased serum superoxide dismutase activity and glutathione level markedly. These results show that ASSR has hypoglycemic, hypotriglyceridemic and antioxidant effects in streptozotocin-induced diabetic rats, suggesting that ASSR supplementation can be useful in preventing diabetic complications associated with hyperlipidemia and oxidative stress.

Acetyl-11-keto-beta-boswellic acid inhibits prostate tumor growth by suppressing vascular endothelial growth factor receptor 2-mediated angiogenesis.

The role of angiogenesis in tumor growth and metastasis is well established. Identification of a small molecule that blocks tumor angiogenesis and is safe and affordable has been a challenge in drug development. In this study, we showed that acetyl-11-keto-beta-boswellic acid (AKBA), an active component from an Ayurvedic medicinal plant (Boswellia serrata), could strongly inhibit tumor angiogenesis. AKBA suppressed tumor growth in the human prostate tumor xenograft mice treated daily (10 mg/kg AKBA) after solid tumors reached approximately 100 mm(3) (n = 5). The inhibitory effect of AKBA on tumor growth was well correlated with suppression of angiogenesis. When examined for the molecular mechanism, we found that AKBA significantly inhibited blood vessel formation in the Matrigel plug assay in mice and effectively suppressed vascular endothelial growth factor (VEGF)-induced microvessel sprouting in rat aortic ring assay ex vivo. Furthermore, AKBA inhibited VEGF-induced cell proliferation, chemotactic motility, and the formation of capillary-like structures from primary cultured human umbilical vascular endothelial cells in a dose-dependent manner. Western blot analysis and in vitro kinase assay revealed that AKBA suppressed VEGF-induced phosphorylation of VEGF receptor 2 (VEGFR2) kinase (KDR/Flk-1) with IC(50) of 1.68 micromol/L. Specifically, AKBA suppressed the downstream protein kinases of VEGFR2, including Src family kinase, focal adhesion kinase, extracellular signal-related kinase, AKT, mammalian target of rapamycin, and ribosomal protein S6 kinase. Our findings suggest that AKBA potently inhibits human prostate tumor growth through inhibition of angiogenesis induced by VEGFR2 signaling pathways.

Morelloflavone, a biflavonoid, inhibits tumor angiogenesis by targeting rho GTPases and extracellular signal-regulated kinase signaling pathways.

Morelloflavone, a biflavonoid extracted from Garcinia dulcis, has shown antioxidative, antiviral, and anti-inflammatory properties. However, the function and the mechanism of this compound in cancer treatment and tumor angiogenesis have not been elucidated to date. In this study, we postulated that morelloflavone might have the ability to inhibit angiogenesis, the pivotal step in tumor growth, invasiveness, and metastasis. We showed that morelloflavone could inhibit vascular endothelial growth factor (VEGF)-induced cell proliferation, migration, invasion, and capillary-like tube formation of primary cultured human umbilical vascular endothelial cells in a dose-dependent manner. Morelloflavone effectively inhibited microvessel sprouting of endothelial cells in the mouse aortic ring assay and the formation of new blood microvessels induced by VEGF in the mouse Matrigel plug assay. Furthermore, morelloflavone inhibited tumor growth and tumor angiogenesis of prostate cancer cells (PC-3) in xenograft mouse tumor model in vivo, suggesting that morelloflavone inhibited tumorigenesis by targeting angiogenesis. To understand the underlying mechanism of morelloflavone on the inhibitory effect of tumor growth and angiogenesis, we showed that morelloflavone could inhibit the activation of both RhoA and Rac1 GTPases but have little effect on the activation of Cdc42 GTPase. Additionally, morelloflavone inhibited the phosphorylation and activation of Raf/mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase/ERK pathway kinases without affecting VEGF receptor 2 activity. Together, our results indicate that morelloflavone exerts antiangiogenic action by targeting the activation of Rho-GTPases and ERK signaling pathways. These findings are the first to reveal the novel functions of morelloflavone in tumor angiogenesis and its molecular basis for the anticancer action.

The protective effect of Yi-Qi-Yang-Yin-Ye, a compound of traditional Chinese herbal medicine in diet-induced obese rats.

The present study was undertaken to determine the effect of Yi-Qi-Yang-Yin-Ye (Y-Q-Y-Y-Y), a compound of Traditional Chinese Herbal Medicine, on insulin resistance (IR) in the diet-induced obese rat model induced by intravenous injection with a low dose of streptozotocin and fed a high fat and high caloric diet. Y-Q-Y-Y-Y (2, 4, 8 g/kg) was administered via gavage daily for 4 weeks. The results showed that Y-Q-Y-Y-Y treatment decreased the levels of body weight, total cholesterol (TC), triglycerides (TG), low density lipoprotein-cholesterol (LDL-C), free fatty acid (FFA), insulin (INS) and fast blood glucose (FBG) and increased the level of high density lipoprotein-cholesterol (HDL-C) in the diet-induced obese rats. Glucose tolerance was improved in the diet-induced obese rats treated with Y-Q-Y-Y-Y as well as GIR (glucose infusion rate) in the hyperinsulinemic euglycemic clamp experiment compared to the model control rats (p < 0.01). Moreover, treatment with Y-Q-Y-Y-Y up-regulated glycogen contents in both liver and skeletal muscle and increased insulin receptor amounts on the erythrocytes surface as assessed by using (125)I-labeled auto-antibodies against insulin receptors. Taken together, our data suggested that Yi-Qi-Yang-Yin-Ye ameliorates insulin resistance in the diet-induced obese rats.

Antihypertensive effect of total flavones extracted from seed residues of Hippophae rhamnoides L. in sucrose-fed rats.

The study was designed to investigate the antihypertensive effect of total flavones extracted from seed residues of Hippophae rhamnoides L. (TFH-SR) and its underlying mechanism in chronic sucrose-fed rats by evaluating its ability to regulate insulin and angiotensin || levels. Feeding of high-sucrose diet (HS: 77% of kcal from carbohydrate, 16% from protein and 6% from lipid, respectively) for 6 weeks resulted in significant rise in systolic blood pressure (SBP) by 25.60%, plasma insulin by 114.24%, triglycerides by 85.14% and activated angiotensin || contents in heart and kidney. However, TFH-SR treatment significantly suppressed the elevated hypertension, hyperinsulinemia and dyslipidemia. Furthermore, TFH-SR (especially at the dose of 150mg/kg/day) increased the circulatory blood angiotensin || level as effective as angiotensin || receptor blocker. These results indicated that TFH-SR exerted its antihypertensive effects at least in part by improving insulin sensitivity and blocking angiotensin || signal pathway. Findings of the present study suggested that TFH-SR might prove to be of potential use in the management of hyperinsulinemia in non-diabetic state with cardiovascular diseases.

[Study on antioxidant activity of pigment of Lycium ruthenicum].

OBJECTIVE: To elvaulate the antioxidant activity of the pigment of Lycium ruthenicum. METHOD: The antioxidant activities were measured by the effects of the reducing ability, scavenging DPPH. H2O2-induced hemolysis of mice erythrocyte, serum resistance of reactive oxygen species, content of MDA in liver tissue, and swelling effect of mitochondria in liver tissue. RESULT: The pigment of L. ruthenicum could scaveng DPPH* remarkably with IC50 0.164 mg x mL(-1), inhibitte hemolysis of mice erythrocyte evidently with IC50 0.112 mg x mL(-1). The resistant of reactive oxygen species was enhanced by the tested substances, simultanously. The concentration of MDA of peroxidation of lipid in mice liver could be reduced, and the swelling of mice liver mitochondria alse be restrained. CONCLUSION: The pigment of L. ruthenicum has antioxidant activity in tested concentration.

[Effect of flavonoids from Hippophae rhamniodes residues on blood lipoid metabolism and antioxidative activity in climacteric rats].

OBJECTIVE: To study the effect of flavonoids from seed residues of Hippophae rhamnoides (FH) on the lipid metabolism and antioxidative activity in climacteric rats. METHOD: Menopausal rats with aging were used in this experiment. The rats were fed with FH by gastrogavage for 13 weeks. The effect of drug on the lipid metabolism and the antioxidative activity were observed after the rats were killed. RESULT: Serum total cholesterol was decreased significantly in rats fed with FH, T-AOC and SOD in serum and liver were significantly higher than those in rats fed with water, and at the same time MDA was lower than that in rats fed with water. CONCLUSION: FH can improve the climacteric rats' lipid metabolism, and enhance the antioxidation in climacteric rats.

[Inhibitory effects of saponins from Tribulus terrestris on alpha-glucosidase in small intestines of rats].

OBJECTIVE: To determine the effects of saponins from Tribulus terrestris (STT) on small intestinal a-glucosidase and postprandial blood glucose levels in rats. METHOD: The inhibitory effects of STT on a-glucosidase extracted from small intestines in rats were carried out in vitro. The blood glucose levels were measured after 60 min when sucrose (2 g x kg(-1)) or glucose (2 g x kg(-1)) was administered orally with STT (100 mg x kg(-1)). After treated with STT (100 mg x kg(-1)) for 14 d, the activities of a-glucosidase were determined daily, as well as the postprandial blood glucose levels after oraly administered sucrose (2 g x kg(-1)). RESULT: STT at concentrations of 0.1, 1 and 10 mg x mL(-1) reduced significantly the activities of alpha-glucosidase with inhibitory rates of (20.83 +/- 1.66)%, (43.73 +/- 2.39)% and (52.62 +/- 2.69)%, respectively. In facts STT (100 mg x kg(-1)) considerably decreased the blood glucose levels which was 52.61% of that of the control in rats co-administered orally with sucrose (2 g x kg(-1)). However, it showed no such effect on the rats co-administered orally with glucose (2 g x kg(-1)). After orally administered of STT for 14 d, the activity of alpha-glucosidase was significantly reduced (P < 0.05) to (58.17 +/- 3.24)% of that those in control. Meanwhile, The rats were oral administered with sucrose, the increase of postprandial blood glucose levels were (69.50 +/- 4.28)% of that in control 60 min later ( P < 0.05). CONCLUSION: It was through inhibiting the activity of a-glucosidase in small intestines that STT significantly retarded the increase in postprandial blood glucose levels in rats.

[Experimental study of saponins from Tribulus terrestris on renal carcinoma cell line].

OBJECTIVE: To investigate the effect of saponins from Tribulus terrestris (STT) on the renal carcinoma cell (786-0) in vitro, and inhibitory mechanisms. METHOD: Effects of SIT on the cytotoxicity, morphological changes of apoptosis, cell cycle and expression of Bcl-2 protein in the 786-0 were tested respectively by MTT method, Wright and acridine orange stain assay, as well as flow cytometry (FCM). RESULT: After the 786-0 was treated by STY, it was shown that: 1) A significant cytotoxic effect was observed by MTT assay; 2) Apoptosis-induced was viewed by Wright and acridine orange stain assay; 3) The distribution of 786-0 on S phase was increased; 4.) The expression of Bcl-2 protein and cyclin D1 was decreased. CONCLUSION: STT can significantly inhibit the growth of 786-0 in vitro, partially, by apoptosis.

[Study on antioxidant activity of essential oils and its monomer from Pelargonium graveolens].

The antioxidant effects of essential oil and monomer as well as residue and waste water after distillation from buds, stems and leaves of Pelargonium graveolens were studied by the method of 1,1-diphenyl-2-picryl hydrazyl free redical (DPPH*). It showed that each sample in the test had the antioxidant effect. The extraction of the leaf collected in noon had the strongest antioxidant effect, the residue and waste water had also strong antioxidant effect. It shows that some antioxidant chemical abounds in the residue of natural essential industry, and it also shows feasibility of integrated use of Pelargonium graveolens.