Effects of tumor necrosis factor and E-selectin on coronary artery flow.

OBJECTIVE: The aim of the study is to investigate the correlation between tumor necrosis factor (TNF-α), E-selectin and coronary artery flow following myocardial ischemia-reperfusion model (IR) in Yorkshire pigs. MATERIALS AND METHODS: Establishment of IR model in pigs. Following the injury model, Experiment group was administrated intravenously Shenfu injection solution (SFI, 1 mL/kg). The control group received the same amount of saline. After 30 min of blood reflux, thrombolysis in myocardial infarction frame count (TFC) was recorded following surgery. TNF-α, E-selectin expression was determined by ELISA in the venous sheath, coronary sinus, artery sinus, and proximal segment of the coronary artery. RESULTS: After the blood reflowing, TFC in both groups were upregulated, and TFC increased more than the control group. The difference is statistically significant (p<0.05) at the time of 30 min. TNF-α, E-selectin expression increased after IR. After reperfusion, TNF-α, E-selectin levels further increased and the myocardial injury was aggravated. SFI inhibited inflammation in the experimental group. TNF-α, E-selectin levels at coronary sinus, artery sinus, and distal segment of coronary artery after surgery was positively correlated with TIMI in the experimental group (p<0.05). TNF-α, E-selectin levels significantly increased after reperfusion (p<0.05). CONCLUSIONS: The result demonstrated that TNF-α, E-selectin levels were positively correlated with coronary artery reflow only in the experimental group but not in the control group.

Correlation study between interleukin-6 levels and coronary reflow.

OBJECTIVE: To analyze the correlation between local interleukin-6 (IL-6) levels in different parts of blood vessel and the record of Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) after myocardial ischemia-reperfusion (IR) model. MATERIALS AND METHODS: Establishment of IR model in Yorkshire pigs, the pigs were divided into two groups (n=6). Experiment group pigs were administrated with Shenfu injection (SF) intravenously (1 mL/kg), control group was given saline injection. The blood reflowed after 30 min. TIMI was recorded to evaluate the coronary blood flow and myocardial perfusion. IL-6 levels in venous sheath, coronary sinus, artery sinus, and proximal coronary artery were determined by ELISA. RESULTS: The records of TIMI in experimental group were higher than that in control group. The difference was statistically significant (p < 0.05). The level of IL-6 increased obviously compared with control group after reperfusion (p < 0.05). Shenfu injection reduced the level of IL-6. IL-6 level at the coronary sinus was positively correlated with TIMI in experimental group (p = 0.03, R2 = 0.97) but not in control group. CONCLUSIONS: IL-6 levels were significantly increased after reperfusion, which aggravated myocardial injury. IL-6 may be associated with coronary reflow, but further study is needed.

The adverse effects of long-term l-carnitine supplementation on liver and kidney function in rats.

Levo-Carnitine (l-carnitine) is widely used in health and food. This study was to focus on the adverse effects of 8-week oral supplementation of l-carnitine (0.3 and 0.6 g/kg) in female and male Sprague Dawley rats. l-carnitine reduced body and fat weights, as well as serum, liver, and kidney lipid levels in rats. Simultaneously, hepatic fatty acid ß-oxidation and lipid synthesis were disturbed in l-carnitine-fed rats. Moreover, l-carnitine accelerated reactive oxygen species production in serum and liver, thereby triggering hepatic NOD-like receptor 3 (NLRP3) inflammasome activation to elevate serum interleukin (IL)-1ß and IL-18 levels in rats. Alteration of serum alkaline phosphatase levels further confirmed liver dysfunction in l-carnitine-fed rats. Additionally, l-carnitine may potentially disturb kidney function by altering renal protein levels of rat organic ion transporters. These observations may provide the caution information for the safety of long-term l-carnitine supplementation.

Protective activity of the ethanol extract of Cynanchum paniculatum (BUNGE) Kitagawa on treating herpes simplex encephalitis.

To date there has been no valid treatment for herpes simplex encephalitis (HSV). This study explores the protective activity of ethanol extract of Cynanchum paniculatum (bunge) kitagawa for treatment of HSV. Cell models and animal models were established and divided into 4 groups: normal group, virus group, cynanchum paniculatum group and Dexamethasone group. Flow cytometry was employed to detect apoptosis of cell model and TUNEL assay was chosen to detect apoptosis of animal tissues. The survival time of the animal models was observed. ELISA was used to measure TNF-alpha expression and the Greiss method to measure Nitric Oxide (NO) expression in the mouse brain. As a result, it was found that extract of Cynanchum paniculatum can improve the survival rate of HSV-infected mice. The extract could prevent apoptosis in the neuron cell model and reduce apoptosis rate in brain tissue after HSV infection. With the extract intervention, TNF-alpha and NO levels in brain tissue were significantly decreased in the animal model. In conclusion, the extract of Cynanchum paniculatum can prevent HSV-inducing impairment in the cell and animal model of HSE.

Inducing-apoptotic activity of the ethanol extract of Duchesnea indica Focke on treatment of herpes simplex encephalitis.

This study explores the inducing-apoptotic activity of the ethanol extract of Duchesnea indica Focke on treatment of herpes simplex encephalitis. Cell models were employed and divided into 4 groups: normal group, virus group, Duchesnea indica group and dexamethasone group. Cytopathic effect examination was employed to detect apoptosis of PC-12 and BV-2 cells. ELISA was used to measure TNF-α, IL-1ß, and Greiss method to measure NO secretion. Flow cytometry assay for caspase-3 expressions was performed. As a result, the ethanol extract of Duchesnea indica could protect the neuron cell model from impairment by virus. In the cell model of microglia stimulated by herpes simplex virus (HSV), with the ethanol extract intervention, TNF-α, IL-1ß and NO levels were significantly decreased and cell death of BV-2 cells were markedly increased. The expression level of caspase-3 was notably elevated after the extract intervention. In conclusion, the ethanol extract of Duchesnea indica can reduce HSV-induced inflammatory injury on neuron due to the induction of microglia apoptosis.

Two new triterpenoid saponins from Sarcandra glabra.

Two new triterpenoid saponins, named sarcandroside A and B, have been isolated from Sarcandra glabra (Thunb) Nakai. Their structures have been established as 3beta,19alpha,20beta-trihydroxyurs-11,13 (18)-diene-28,20beta-lactone-3-O-beta-D-glucopyranosyl (1 --> 3)-[alpha-L-rhamnopyranosyl(1 --> 2)]-beta-D-xylopyranoside (1) and 3-O-beta-D-glucopyranosyl (1 --> 3)-[alpha-L-rhamnopyranosyl(1 --> 2)]-beta-D-xylopyranosyl-pomolic acid 28-O-beta-D-glucopyranosyl ester (2) by means of spectral and chemical methods.

Mutation of conserved aspartates affect maturation of presenilin 1 and presenilin 2 complexes.

Presenilin (PS1 and PS2) holoproteins are transiently incorporated into low molecular weight (MW) complexes. During subsequent incorporation into a higher MW complex, they undergo endoproteolysis to generate stable N- and C-terminal fragments (NTF/CTF). Mutation of either of two conserved aspartate residues in transmembrane domains inhibits both presenilin-endoproteolysis and the proteolytic processing of APP and Notch. We show that aspartate-mutant holoprotein presenilins are not incorporated into the high molecular weight, NTF/CTF-containing complexes. Aspartate-mutant presenilin holoproteins also preclude entry of endogenous wild-type PS1/PS2 into the high molecular weight complexes, but do not affect the incorporation of wild-type holoproteins into lower molecular weight holoprotein complexes. These data suggest that the loss-of-function aspartate-mutants cause altered PS complex maturation, and argue that the functional presenilin moieties are contained in the high molecular weight presenilin NTF/CTF-containing complexes.

Electron probe X-ray microanalysis of otoconia in the guinea pig inner ear.

By using the electron probe X-ray microanalysis technique, the elemental composition of otoconia was analyzed in the normal adult pigmented guinea pig. In the X-ray spectra of otoconia, the most abundant element was Ca, but significant peaks for P, S, Cl and K were also detected. The comparison of the elemental composition in the utricular and saccular otoconia did not show any significant difference. Regression analysis revealed that the concentrations of Ca and K are related by a linear function in both the utricular and saccular otoconia. Analysis of otoconia of different sizes showed that there were no differences in Ca concentration in small, normal and large otoconia. The comparison of other elemental compositions revealed that P, S, Cl and K in the central part of saccular small otoconia showed higher concentrations than those of normal or large otoconia. P, S, Cl and K in the utricular small otoconia showed relatively higher concentrations. These findings may indicate that the small otoconia are immature or newly generated.

Araliasaponins XII-XVIII, triterpene saponins from the roots of Aralia chinensis.

Seven new oleanane-type saponins, named araliasaponins XII-XVIII, were isolated from the roots of Aralia chinensis, together with 14 known triterpene saponins. On the basis of the chemical and spectroscopic evidence, the structures of these new saponins were elucidated as follows: 3-O-beta-D-glucopyranosyl(1-->3)-[beta-D -glucopyranosyl(1-->2)]-alpha-L-arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl(1-->3)-[beta-D-xylopyranosyl (1-->2)]-alpha-L-arabinopyranosyl oleanolic acid 28-O-alpha-L-rhamnopyranosyl(1-->4)-beta-D-glucopyranosyl (1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D -glucopyranosyl(1-->3)-[beta-D-galactopyranosyl(1-->2)] -beta-D-glucopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl(1-->3)-[beta-D -xylopyranosyl(1-->2)]-beta-D-glucopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl (1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D -glucopyranosyl(1-->3)-[beta-D-galactopyranosyl (1-->2)]-beta-D-galactopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-alpha-L -arabinofuranosyl(1-->4)-[beta-D-glucopyranosyl (1-->2)]-beta-D-glucuronopyranosyl oleanolic acid dimethyl ester and 3-O-alpha-L-arabinofuranosyl (1-->4)-[beta-D-glucopyranosyl(1-->2)]-beta-D -glucuronopyranosyl oleanolic acid 28-O-beta-D -glucopyranosyl(1-->6)-beta-D-glucopyranosyl methyl ester, respectively.

Araliasaponins I-XI, triterpene saponins from the roots of Aralia decaisneana.

Seven new oleanane-type and four new ursane-type triterpene saponins, named araliasaponins I-XI were isolated from the roots of Aralia decaisneana, together with four known triterpene saponins. On the basis of the chemical and spectroscopic evidence, the structures of these new saponins were elucidated as follows: 3-O-beta-D-xylopyranosyl-(1-->3)-beta-D- glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-alpha-L- arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-alpha-L- arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D- glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D- xylopyranosyl-(1-->2)]-alpha-L-arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-beta-D- glucopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-beta-D- galactopyranosyl oleanolic acid, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D- xylopyranosyl-(1-->2)]-beta-D-galactopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-beta-D- galactopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]- alpha-L-arabinopyranosyl ursolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-alpha-L - arabinopyranosyl ursolic acid, 3-O-beta-D-glucopyranosyl-(1-->3)-alpha-L-arabinopyranosyl ursolic acid 28- O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester and 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]- beta-D-glucopyranosyl ursolic acid 28-O-beta-D-glucopyranosyl ester.

[Structure modification of triptolide, a diterpenoid from Tripterygium wilfordii].

In this paper, the structure modification of triptolide was studied and nine triptolide derivatives were synthesized. A preliminary test for the immunosuppression activity in vitro showed that tripchlorolide (2) and tripbromolide (3) have strong activity similar to triptolide, while their toxicity are much lower. The activity of other compounds was decreased significantly. A simple method for the preparation of tripchlorolide from triptolide in 92% yield was found by reacting triptolide with HCl in acetone under mild condition.

[The structure of tripterygone].

Three triterpene compounds have been isolated from the roots of Tripterygium wilfordii Hook F. The structure of the new compound, 3-hydroxy-25-norfriedel-3, 1 (10)-dien-2-one-30 oic acid named tripterygone (III), and the identity of others, 3 beta, 22 beta-dihydroxy-delta 12-oleanen-29-oic acid (I) and 2 alpha, 3 alpha, 24-trihydroxy-delta 12-ursene-28-oic acid (II) have been established by spectral data and physical properties. Compound II was isolated for the first time from the title plant.

Structure of Tripterygic Acid A: A New Triterpene of Tripterygium wilfordii.

From roots of TRIPTERYGIUM WILFORDII used in Chinese folk medicine, a new ursane-triterpene named tripterygic acid A was isolated along with a known triterpene and their structures were elucidated by means of spectral analysis and chemical transformation.