[Effect analysis of the modified wire-loop snare technique in retrieving severely tilted inferior vena cava filters].

Objective: To examine the application effect of the modified wire-loop snare technique in retrieving severely tilted inferior vena cava filters (IVCF). Methods: The clinical data of 18 patients (12 males and 6 females, aged (62.1±13.1) years (range: 29 to 78 years)) who underwent the modified wire-loop snare technique to retrieve IVCF at the Affiliated Hospital of Qingdao University, Qingdao Eighth People's Hospital, and Jimo District Hospital of Traditional Chinese Medicine from November 2017 to April 2022 were retrospectively analyzed. The applied filters included drum-type filters (OptEase in 7 cases, Aegisy in 2 cases) and conical filters (Celect in 6 cases and Denali in 3 cases). Preoperative CT angiography and intraoperative digital subtraction angiography showed that the filter was severely tilted and the hook was covered by hyperplastic intima of the vena cave vein. A modified wire-loop snare technique was used to retrieve drum-type filters and conical filters via femoral and jugular vein approaches, respectively. After successful puncture, the long sheath was placed, the 4 F (1 F≈0.33 mm) vertebral catheter and a snare were inserted through the long sheath, and the 5 F pigtail catheter was inserted simultaneously to guide a 0.035 inch soft guide-wire (260 cm in length) to pass through the top of the filter and turning back. The tip of the soft guide-wire was snared by the vertebral catheter and pulled out of the sheath. The 4 F vertebral catheter was inserted following the tip of the guide-wire to form a wire-loop using the vertebral catheter and the pigtail catheter. After fixing the tip and tail of the soft guide-wire in vitro, the long sheath was pushed forward to cut the hyperplastic intima and the hook was pulled away from the vena cava wall to retrieve the filter under the support of two catheters. Results: The filters were successfully retrieved in 17 cases, the operation time was (25.5±8.7) minutes (range: 15 to 45 minutes), no complication occured. The hook of one filter (Celect) penetrated out of the vena vava wall and the wire-loop could not pull the hook back into the vena cava. Then the filter was removed by laparotomy. Conclusion: The modified wire-loop snare technique could retrieve the severely tilted retrivable drum-type filters and conical filters, even when serve adhesion exists between the filter and the vena cava wall.

Effectiveness of amendments on re-acidification and heavy metal immobilization in an extremely acidic mine soil.

Previous studies have shown that the application of soil amendments is efficient in reducing acidity and heavy metal bioavailability in mine soils. However, it remains a challenge for environmentalists to predict accurately and control economically the re-acidification in re-vegetated mine soils. In this study, net acid generation (NAG) test and bioassay technique were employed to assess the effectiveness of the amendments [including lime, N-P-K (nitrogen, phosphorous and potassium) fertilizer, phosphate and river sediment] on re-acidification and heavy metal immobilization in an extremely acid (pH < 3) mine soil. Our results suggested that NAG test was a rapid and accurate approach to assess the effectiveness of the amendments on re-acidification potential of the mine soil. Interestingly, it was found that phosphate and river sediment played quite specific roles in preventing the re-acidification in the mine soil. In addition, the results also indicated that the addition of 25 t ha(-1) lime combined with river sediment (30%) might be an economical method to successfully control the acidification and re-acidification in the extremely acid mine soil, allowing the re-establishment of the plants. Collectively, our results implied that the combined use of NAG test and bioassay assessment was effective in evaluating a reclamation strategy for extremely acidic mine soils.

Effect of 17beta-oestradiol and ginsenoside on osteoporosis in ovariectomised rats.

To study the anti-osteoporosis effects and mechanism of action of oestradiol (E2) and ginsenoside (tR), we measured the bone mineral densities (BMD) of lumbar vertebra and tibia and analysed the tibia histological morphological data, as well observed the activity and the number of osteoblasts and the activity of alkaline phosphatase (ALP) and the concentration of cAMP. Results showed that E2 (400 microg kg- 1 week- 1) and tR (10, 20, 30 mg kg- 1 day- 1) were able to countervail the decreasing in BMDs of lumbar vertebra and tibia induced by OVX in rats (P<0.05); E2 (0.1 micromol l- 1) and ginsenoside Rg1 (1 micromol l- 1 and 10 micromol l- 1) were able to increase the number of osteoblasts, the activity of ALP and the concentration of intercellular cAMP in cultured osteoblast cells. The present findings suggest that E2 and tR have an anti-osteoporosis effect in ovariectomised rats.

New drugs derived from medicinal plants.

In China, increasing emphasis has been laid in recent years on research on natural products. About 140 new drugs have been developed from Chinese medicinal plants. For example, anisodamine possesses good effects in the treatment of septic shock and morphine addiction; 3-n-butylphthalide isolated from seeds of celery was shown to be a new cerebral anti-ischemic agent; indirubin was identified as an anti-leukemic drug with no inhibition of bone marrow; huperzine is a potent and reversible inhibitor of acetylcholinesterase (AChE) and its selective action is superior to that of donepezil; clausenamide was shown to be a potassium channel blocker, its nootropic effect was 50-100 times more potent than that of piracetam; bicyclol was synthesized from schizandrin C isolated from Fructus schizandrae. It has remarkable hepatoprotective and certain anti-hepatitis virus actions; salvianolic acid B is a very strong antioxidant agent with potential anti-dementia effects; yingzhaosu A and artemisinin are anti-malaria drugs containing a peroxide ring which is very rarely seen in natural substances.

Salvianolic acid B inhibits fibril formation and neurotoxicity of amyloid beta-protein in vitro.

AIM: To observe the effect of salvianolic acid-B (SalB) on amyloid beta-protein (A-beta) fibril formation and its toxicity towards PC12 cells. METHODS: A-beta (1 - 40) was incubated with or without SalB at 25 degrees C for 30 h, 48 h, and 100 h. Fibril formation was then viewed under an electron microscope. Toxicity of the A-beta (1 - 40) towards PC12 cells was measured with 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). A-beta (25 - 35) was aged by incubating at 25 degrees C for 7 d, then the peptide was incubated with PC12 cells with or without SalB. Toxicity of A-beta (25-35) towards PC12 cells was observed with MTT. RESULTS: Following incubation at 25 degrees C for 30 h, A-beta (1 - 40) (100 mg/L) aggregated and formed fibrils. SalB 10-100 nmol/L completely prevented the fibril formation within 30 h. Extension of amyloid fibrils increased with prolonging the incubation time. SalB inhibited the fibril formation process during this period. In the MTT assay A-beta (1 - 40) incubated with SalB manifested significantly lower toxicity to PC12 cells compared with that without SalB. Besides, SalB 1 micromol/L significantly attenuated the toxicity of aged A-beta (25 - 35) to PC12 cells. CONCLUSION: SalB could inhibit A-beta aggregation and fibril formation, as well as directly inhibit the cellular toxicity of aged A-beta towards PC12 cells.

[Effects of salvianolic acid B on beta-amyloid peptide neurotoxicity of primary cultured fetal rat cortical neurons].

AIM: To study the roles of nitric oxide (NO) and nitric oxide synthase (NOS) on the glutamate (Glu) and beta-amyloid peptide [beta-AP (1-40)] mediated neurotoxicity in primary cultured fetal rat cortical neuron and the neuroprotective effects of salvianolic acid B (Sal B) against the beta-AP (1-40) and its mechanism of action. METHODS: With application of specific agonist and antagonist of NOS, establishment of the sodium nitroprusside (SNP), Glu and beta-AP (1-40) neurotoxicity model, the cell viability, lactate dehydrogenase (LDH) efflux and NO release were detected by using morphological observation, MTT stain, spectrophotometric measurement and Griess method, respectively, in primary cultured fetal rat cortical neurons. RESULTS: Glu and beta-AP (1-40) were shown to increase the NO release of the neuron. Furthermore, nNOS was found to play an important role in the neurotoxicity of glutamate, iNOS may probably be involved in the neurotoxicity of beta-AP (1-40). Sal B (0.01, 0.10, 1.00 microgram.L(-1)) was shown to increase the cell viability, decrease the LDH release rate and inhibit NO release in a dose-dependent manner. CONCLUSION: These results suggest that the neurotoxicity of Glu and beta-AP(1-40) may be partly mediated through different types of NOS. Sal B was found to prevent the beta-AP(1-40) toxicity by directly or indirectly decreasing NO release.

Effects of 7-nitroindazole on long-term potentiation induced by l-clausenamide and high-frequency stimulation in rat hippocampus in vivo.

AIM: To study the antagonistic effect of selective neuronal nitric-oxide synthase (nNOS) inhibitor 7-nitroindazole on the long-term potentiation (LTP) induced by l-clausenamide (Cla) in rat hippocampus in vivo. METHODS: Population spike (PS) of evoked potentials was determined by extracellular recording technique in the hippocampal dentate gyrus (DG) of anesthetized rats. RESULTS: 7-Nitroindazole 2 nmol icv blocked the induction of LTP elicited by high-frequency (100 Hz) stimulation or Cla 5 nmol icv (P < 0.01), and L-arginine 225 mg.kg-1 i.p. prevented the action of 7-nitroindazole (P < 0.01). CONCLUSION: Nitric oxide produced by nNOS plays a role in the induction of Cla-induced LTP in hippocampus.

Effects of naloxone on l-clausenamide-induced long-term potentiation in dentate gyrus of anesthetized rats.

AIM: To investigate the mechanisms of l-clausenamide-induced long-term potentiation (LTP) in the dentate gyrus of anesthetized rats. METHODS: Extracellular recording technique was used to record the population spike (PS) in the dentate gyrus of anesthetized rats. RESULTS: I.c.v. injection of naloxone 1 nmol, affecting neither the basal PS amplitude nor the LTP induced by tetanus, reduced the l-clausenamide-potentiated LTP only when it was administrated prior to clausenamide. Naloxone 1 nmol (i.c.v.), administrated 10 min before l-clausenamide, reduced the PS amplitude at 20 min, 55 min, and 90 min after i.c.v. injection of l-clausenamide 4 nmol from 138% +/- 10%, 170% +/- 10%, and 169% +/- 12% to 111% +/- 7%, 124% +/- 14%, and 123% +/- 11%, respectively. All P < 0.01 (n = 8). The same dose of naloxone (i.c.v.), delivered 10 min after l-clausenamide, did not affect the l-clausenamide-induced potentiation. CONCLUSION: The activation of opioid receptors contributes to the induction of l-clausenamide-induced LTP of synaptic transmission in dentate gyrus of anesthetized rats.

Inhibitory effect of resveratrol on interleukin 6 release by stimulated peritoneal macrophages of mice.

In the present investigation, interleukin 6 (IL-6) activity in the supernatant of cultured mouse peritoneal macrophages was monitored using a sensitive bioassay involving the IL-6-dependent murine hybridoma B9 cell line. The effects of resveratrol on Il-6 release by mouse peritoneal macrophages stimulated with calcium ionophore A23187 and fMLP were explored. Resveratrol, at a concentration range from 5 x 10(-6) to 4 x 10(-5) mol.l-1, was found to dose-dependently inhibit IL-6 release by cultured macrophages induced by A23187 and fMLP, and showed no direct cytotoxic effect, but induced proliferation of cultured mouse thymus cells. Resveratrol, at a concentration range from 10(-8) to 10(-5) mol.l-1, was shown to dose-dependently inhibit calcium ion influx into the cells with the stimulation of fMLP (10(-6) mol.l-1). These results suggest that the blocking of calcium ion influx into cells by reveratrol is one of the possible mechanisms of the IL-6 biosynthesis inhibitory action of resveratrol.

Effect of 17-beta-estradiol and ginsenoside Rg1 on reactive microglia induced by beta-amyloid peptides.

The reactive microglias induced by 25 micromol of beta-amyloid peptides (Abeta25-35) and/or IFN-gamma can initiate the microglial respiratory burst and release NO, respectively. Oxidative stress and inflammatory function have been implicated in Alzheimer's disease (AD). We showed that 10 micromol 17-beta-estradiol (E2) and 1-10 micromol ginsenoside Rg1 (Rg1) could prevent the toxicity of Abeta25-35 and/or IFN-gamma to microglias, inhibit the microglial respiratory burst activity and decrease the accumulation of NO. These results demonstrated the protectional effect of E2 or Rg1 on neuron from damaging by reactive microglias in AD.

Effects of dl-3-n-butylphthalide on regional cerebral blood flow in right middle cerebral artery occlusion rats.

AIM: To study the effect of dl-3-n-butylphthalide (NBP) on regional cerebral blood flow (rCBF) in forcal cerebral ischemia rats. METHODS: In chloral hydrate-anesthetized rat, the proximal portion of right middle cerebral artery (RMCA) was occluded, and H2 needle electrode was implanted in right striatum. rCBF was monitored in striatum using hydrogen clearance method. RESULTS: Ten min after RMCA occlusion (RMCAO), NBP (5, 10, 20 mg.kg-1 i.p.) markedly increased rCBF to striatum (P < 0.01). When NBP was given i.p. 40 min after RMCAO, the increasing effect on rCBF was also observed (P < 0.05). However, when NBP was injected i.p. 60 min after RMCAO, the increasing effect of NBP on rCBF was not found. In NBP-pretreated (i.p. 40 min before RMCAO) group, rCBF in striatum measured at different time points of 30, 60, 90, 120, 150, and 180 min after RMCAO were increased by 97%, 107%, 136%, 211%, 173%, and 317%, respectively, compared with the percentages of vehicle group. The potency of the effect of Nim (0.5 mg.kg-1 i.p.) was similar to that of NBP (10 mg.kg-1 i.p.). CONCLUSION: NBP pre-treatment or post-treatment markedly enhanced the rCBF to striatum in RMCAO rats.

Stimulation of central cholinergic neurons by (-)clausenamide in vitro.

AIM: To study the neurotrophic effects of (-) and (+)clausenamide on frontal cortex neurons in culture. METHODS: The activity of the choline acetyltransferase (ChAT) was determined by spectrophotometric method; protein content was assayed by Folin phenol method. RESULTS: (-)Clausenamide increased the activity of ChAT and protein content in cultured neurons, as well as stimulated proliferation of neuronal cells, support survival and neurite outgrowth of neurons. The neurotrophic action of (-)clausenamide (0.001-10 mumol.L-1) was similar to that of nerve growth factor. The (+)clausenamide had no neurotrophic action, even at high concentrations (0.1-10 mumol.L-1), but neurons were damaged. CONCLUSION: (-)Clausenamide stimulated central cholinergic neuron development.

[Study on the anti-apoptotic mechanism of ginsenoside Rg1 in cultured cortical neurons].

Ginsenoside Rg1 is an active principle isolated from Panax ginseng CA Meyer. Primary neuronal culture was performed with different concentrations of Rg1. On the 14th day, the culture was changed to serum-free medium. On the 16th day, neurons were harvested and assayed under microscope and fluorescence microscope. The result showed that serum withdrawal from the medium induced apoptosis in primary cultured cortical neurons. Rg1 (1, 10 mumol.L-1) was shown to inhibit apoptosis and protect neurons against injury. Membrane fluidity was measured using fluorescence spectrophotometer in five groups of cultured cortical neurons: control (complete medium), apoptosis (serum-free medium), Rg1 0.1 mumol.L-1, Rg1 1 mumol.L-1 and Rg1 10 mumol.L-1. Neurons were isolated enzymatically and loaded with the fluorescent dye, DPH (1, 6-diphenyl-1,3,5-hexatriene). Membrane fluidity in control neurons (eta 1.2928 +/- 0.1426) was shown to be significantly higher than that in apoptosis cells (eta 2.9277 +/- 0.2004). The membrane fluidity of neurons treated with Rg1 (0.1, 1, 10 mumol.L-1) increased significantly (eta 2.9172 +/- 0.1604, 2.4731 +/- 0.2187, 1.6436 +/- 0.1483). These findings indicate a substantial alteration of membrane fluidity with neuronal apoptosis. Increment of membrane fluidity provides an aspect of elucidating the mechanism of Rg1's anti-apoptosis function.

[Effect of age and ginsenoside Rg1 on nitric oxide content and nitric oxide synthase activity of cerebral cortex in rats].

Nitric oxide(NO) content and nitric oxide synthase(NOS) activity were measured in cerebral cortex isolated from Wistar rats of three age groups(young: 3 months; adult: 9 months; and old: 27 months). No significant differences in NO content and NOS activity between young and adult rats were found(P > 0.05). The NO content and NOS activity in old rats were shown to be significantly higher than those of young and adult rats(P < 0.01). When treated with Rg1(10, 20, 40 mg.kg-1), the NO content and NOS activity in old rats decreased. The inhibitory effect of Rg1 on NOS was found to be dose-dependent in the range of 10-40 mg.kg-1. The optimal reduction in NO content and NOS activity induced by Rg1 occurred at 40 mg.kg-1 for old rats(P < 0.01). In view of the close relationship of NO content and NOS activity with aging, the inhibitory effect of Rg1 on NOS activity, as shown by our results, might provide an explanation for its antiaging function.

[Effects of age and ginsenoside RG1 on membrane fluidity of cortical cells in rats].

Membrane fluidity was measured using fluorescence spectrophotometer in cortical cells isolated from Wistar rats of five age groups (fetal); neonatal (3 days), young (3 months), adult (9 months) and old (27 months). Neurons were enzymatically isolated and loaded with the fluorescent dye, DPH (1,6-diphenyl-1,3,5-hexatriene). The membrane fluidity of neonatal cells was shown to be significantly higher (eta 1.485 +/- 0.211) than that in young cells (eta 2.220 +/- 0.169), and that in young cells was significantly higher than that in old cells (eta 2.842 +/- 0.143). No significant difference in fluidity, neither between fetal and neonatal cortical cells nor between young and adult ones was observed. Ginsenoside Rg1 (Rg1) is one of the important active principles of ginseng and shares many pharmacological effects of this plant. When treated with Rg1 (10, 20, 40 mg.kg-1), the membrane fluidity of old cortical cells significantly increased (eta 2.670 +/- 0.108, 2.381 +/- 0.123, 2.000 +/- 0.101). These findings indicate a substantial alteration of membrane fluidity with neuronal aging. Increment of membrane fluidity provides an aspect in elucidating the mechanisms of Rg1's antiaging action.

Effects of ginsenoside Rg1 on c-fos gene expression and cAMP levels in rat hippocampus.

AIM: To study the mechanisms of Rg1 antiaging and nootropic function. METHODS: Using Northern and Western blot analyses, the levels of c-fos mRNA and fos protein were determined in the hippocampus of young and old rats treated with or without ginsenoside Rg1. RESULTS: The expression of c-fos gene and protein was decreased in the hippocampus of aged rats, but dose-dependently increased in young and aged rats after the administration of Rg1. Furthermore, Rg1 increased the level of cAMP in the hippocampus of both young and old rats. CONCLUSION: The changes at the genomic and protein levels, arisen from the increase of cAMP, provide an explanation of the mechanisms of Rg1 nootropic and antiaging function. The c-fos proto-oncogene is the prototype of the early-response class of genes. It encodes for a nuclear phosphoprotein, which after forming a complex with the protein product of another oncogene c-jun, binds to the AP-1 sites of DNA, and acts as a regulatory factor for gene transcription. The c-fos gene expression can be considered as a marker for neuronal activity. Moreover, fos protein is believed to be involved in processes related to neuronal plasticity. Ginsenoside Rg1 is one of the important pharmacological principles of ginseng and shares many pharmacological effects of this plant, such as, facilitating learning and memory, and alleviating many ailments, especially those associated with aging. Since the c-fos gene expression might be of crucial importance for neuronal activity and cAMP is a factor regulating gene expression. The present work was to study the effects of Rg1 on c-fos mRNA and protein expression as well as cAMP and cGMP levels.

[Studies on the mechanisms of immunoregulatory effects of ginsenoside Rg1 in aged rats].

Using methods of fluorescence flow cytometry and Western blot analysis, Rg1 was found to enhance the expression of IL-2 receptor alpha chain and inhibit the release of soluble IL-2 receptor. In in vitro experiment, Rg1 showed no influence on Con A-induced increase of cytoplasmic free calcium concentration, but significantly increased the levels of intracellular cAMP and cGMP in aged animals. In view of the important role of cAMP and cGMP as second messengers in the regulation of immune system, the results of the present studies suggest that one of the mechanisms by which Rg1 enhances immune function in old rats might be mediated by increase of cAMP and cGMP contents, resulting in IL-2 gene expression and splenocyte proliferation.

[Immunoregulatory effects of ginsenoside Rg1 in aged rats].

It has been well documented that the immune function declines with age in the human and animals. The possible causes for the decline are the inability of lymphocytes to proliferate in response to mitogenic stimulation and the decrease of IL-2 production. In the present studies, Rg1 was shown to selectively enhance the proliferation of lymphocytes and the production of IL-2 in aged rats. Using Northern blot and Western blot analyses, Rg1 was found to promote IL-2 gene expression which showed increase of IL-2 mRNA and IL-2 protein contents. Interestingly, under the same conditions, studies were carried out on the effect of Rg1 on the immune function of young adult rats, but no marked influence was observed. According to these results, it is reasonable to consider Rg1 an immunoregulator rather than a purely "immunopotentiating agent".