气相色谱-串联质谱法快速筛查人参中192种农药残留

目的:利用气相色谱-串联质谱(GC-MS/MS)检测技术,建立了人参中192种农药多残留的快筛方法,并对11批样品(包括西洋参、人参、红参、生晒参)进行测定。方法:根据风险控制的原则,选择了人参种植实际使用农药、我国禁限用及高毒农药品种作为检测指标,共计192种。样品经乙腈超声提取浓缩后,在多反应监测模式(MRM)下进行检测,并采用分析保护剂-内标法定量以提高结果的准确性。其中对提取溶剂、净化方法[包括固相萃取法和快速样品前处理技术(Quechers)法]及色谱质谱条件都进行了考察和优化。结果:以人参为考察对象,本方法在1~100μg·L~(-1)线性良好,相关系数r0.990,在5,20,100μg·kg-1三水平进行加样回收率考察,98%的农药的平均回收率在70%~120%。11批样品中共检出14种农药单体,其中五氯硝基苯(PCNB)的检出率最高,按照2015年版《中国药典》人参、西洋参项下农残限度要求,不合格率达36%。结论:该方法检测指标针对性强,准确,快速,适用于人参中农药多残留的日常快速筛查。     

Ginseng integrative supplementation for seasonal acute upper respiratory infections: A systematic review and meta-analysis

BackgroundThe aim of the review was to assess whether ginseng can be a useful supplementation for seasonal acute upper respiratory infections (SAURIs).MethodsAll clinical studies investigating ginseng efficacy for the treatment or prevention of SAURIs were included in the review. Medline, EMBASE, Web of Science, Scopus, Cochrane Library, Google Scholar were systematically screened for relevant articles up to May 26th, 2020. The risk of bias was assessed with the Cochrane tool (RoB 2).ResultsNine articles (describing ten trials about P. ginseng or P. quinquefolius) were included in the review. Evidence globally indicated some useful activity of intervention when administered in adjunct to influenza vaccination. The results of our quantitative synthesis suggested a significant effect on SAURIs incidence (RR = 0.69 [95 % C.I. 0.52 to 0.90], p < 0.05), as well as a significant reduction of their duration if only studies with healthy individuals were included in the analysis (MD=-3.11 [95 % C.I.−5.81 to -0.40], p < 0.05). However, the risk of bias was high-to-unclear for most included trials, and publication bias couldn't be excluded.DiscussionLimitations of existing evidence don’t allow to draw conclusions on the topic. Nevertheless, it is not excluded that ginseng supplementation in adjunct to influenza vaccination and standard care might be useful for SAURIs prevention and management in healthy adult subjects, but further high-quality trials are needed to support this hypothesis.OtherThis research was not funded. The protocol was registered in PROSPERO under the following code: CRD42020156235.     

Antiplatelet and antithrombotic activities of Korean Red Ginseng

The antiplatelet and antithrombotic activities of Korean Red Ginseng (KRG) were examined on rat carotid artery thrombosis in vivo, and platelet aggregation in vitro and ex vivo. Administration of KRG to rats not only prevented carotid artery thrombosis in vivo in a dose-dependent manner, but also significantly inhibited ADP- and collagen-induced platelet aggregation ex vivo, while failed to prolong coagulation times such as activated partial thromboplastin time (APTT) and prothrombin time (PT), indicating the antithrombotic effect of KRG might be due to its antiplatelet aggregation rather than anticoagulation effect. In line with the above observations, KRG inhibited U46619-, arachidonic acid-, collagen- and thrombin-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC50 values of 620 +/- 12, 823 +/- 22, 722 + 21 and 650 +/- 14 microg/mL, respectively. Accordingly, KRG also inhibited various agonists-induced platelet serotonin secretions as it suppressed platelet aggregation. These results suggest that KRG has a potent antithrombotic effect in vivo, which may be due to antiplatelet rather than anticoagulation activity, and KRG intake may be beneficial to the individuals with high risks of thrombotic and cardiovascular diseases.     

A ginseng saponin metabolite-induced apoptosis in HepG2 cells involves a mitochondria-mediated pathway and its downstream caspase-8 activation and Bid cleavage

20-O-(beta-D-glucopyranosyl)-20(S)-protopanaxadiol (IH901), an intestinal bacterial metabolite of ginseng saponin formed from ginsenosides Rb1, Rb2, and Rc, is suggested to be a potential chemopreventive agent. Here, we show that IH901 induces apoptosis in human hepatoblastoma HepG2 cells. IH901 led to an early activation of procaspase-3 (12 h posttreatment), and the activation of caspase-8 became evident only later (18 h posttreatment). Caspase activation was a necessary requirement for apoptosis because caspase inhibitors significantly inhibited cell death by IH901. Treatment of HepG2 cells with IH901 also induced the cleavage of cytosolic factors such as Bid and Bax and translocation of truncated Bid (tBid) to mitochondria. A time-dependent release of cytochrome c from mitochondria was observed, which was accompanied by activation of caspase-9. A broad-spectrum caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (zVAD-fmk), and a specific inhibitor for caspase-8, N-benzyloxycarbonyl-Ile-Glu-Thr-Asp-fluoromethylketone (zIETD-fmk), abrogated Bid processing and translocation, and caspase-3 activation. Cytochrome c release was inhibited by zVAD-fmk, however, the inhibition by zIETD-fmk was not complete. The activation of caspase-8 was inhibited not only by zIETD-fmk but also by zVAD-fmk. The results, together with the kinetic change of caspase activation, indicate that activation of caspase-8 occurred downstream of caspase-3 and -9. Our data suggest that the activation of caspase-8 after early caspase-3 activation might act as an amplification loop necessary for successful apoptosis. Primary hepatocytes isolated from normal Sprague-Dawley rats were not affected by IH901 (0-60 microM). The very low toxicity in normal hepatocytes and high activity in hepatoblastoma HepG2 cells suggest that IH901 is a promising experimental cancer chemopreventive agent.     

Neuroprotective actions of the ginseng extract G115 in two rodent models of Parkinson's disease

The herbal remedy, ginseng, has recently been demonstrated to possess neurotrophic and neuroprotective properties, which may be useful in preventing various forms of neuronal cell loss including the nigrostriatal degeneration seen in Parkinson's disease (PD). In these studies, we examine the potential neuroprotective actions of the ginseng extract, G115, in two rodent models of PD. Animals received oral administration of G115 prior to and/or following exposure to the parkinsonism-inducing neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), in mice, or its toxic metabolite, 1-methyl-4-phenylpyridinium (MPP(+)), in rats. Such treatment significantly and dramatically blocked tyrosine hydroxylase-positive cell loss in the substantia nigra and reduced the appearance of locomotor dysfunction. Thus, oral administration of ginseng appears to provide protection against neurotoxicity in rodent models of PD. Further examination of the neuroprotective actions of ginseng and its various elements may provide a potential means of slowing the progress of PD.     

Protective effect of ginsenoside Rg1 on MPP<Superscript>+</Superscript>-induced apoptosis in SHSY5Y cells

Summary. The neuroprotective mechanism of Rg1 was studied in this paper by means of its obvious anti-apoptotic effect on human SHSY5Y cells. SHSY5Y cells were treated with MPP⁺ (1-methyl-4-phenyl-pyridinium) for 72 hours to induce apoptosis. During the apoptosis, production of reactive oxygen species (ROS), activation of c-Jun N-terminal kinase (JNK) and activation of caspase-3 were observed. The results showed that the signal transduction pathway of MPP⁺-induced apoptosis might be ROS to JNK, then to caspase-3. MPP⁺-induced apoptosis in SHSY5Y cells was obviously inhibited in both NAC (N-acetylcysteine) pretreated groups and Rg1 pretreated groups. Meanwhile, compared to that of the controls, our results showed decreased level of ROS, less JNK activity and lower expression of cleaved caspase-3 in pretreated NAC groups and in Rg1 pretreated groups. The protection by Rg1 might be mediated by removing of ROS. The removal of ROS might inhibit the activity of JNK and the expression of cleaved caspase-3. These results suggest that ginsenoside Rg1 may take effect through its anti-apoptotic activity in neurodegenerative diseases.Received October 16, 2002; accepted March 5, 2003 Published online May 28, 2003     

Effects of ginsenosides on Ca channels and membrane capacitance in rat adrenal chromaffin cells

We investigated the effects of ginseng total saponins (GTS) and five ginsenosides on voltage-dependent Ca²⁺ channels and membrane capacitance using rat adrenal chromaffin cells. In this study, cells were voltage-clamped in a whole-cell recording mode and a perforated patch-clamp technique was used. The inward Ca²⁺ currents (I_Ca) was elicited by depolarization and the change in cell membrane capacitance (ΔC_m) was monitored. The application of GTS (100 μg/ml) induced rapid and reversible inhibition of the Ca²⁺ current by 38.8 ± 3.6% (n = 16). To identify the particular single component that seems to be responsible for Ca²⁺ current inhibition, the effects of five ginsenosides (ginsenoside Rb₁, Rc, Re, Rf, and Rg₁) on the Ca²⁺ current were examined. The inhibitions to the Ca²⁺ current by Rb₁, Rc, Re, Rf, and Rg₁ were 15.3 ± 2.2% (n = 5); 36.9 ± 2.4% (n = 7); 28.1 ± 1.9% (n = 12); 19.0 ± 2.5% (n = 10); and 16.3 ± 1.6% (n = 15), respectively. The order of inhibitory potency (100 μM) was Rc > Re > Rf > Rg₁ > Rb₁. A software based phase detector technique was used to monitor membrane capacitance change (ΔC_m). The application of GTS (100 μg/ml) induced inhibitory effects on ΔC_m by 60.8 ± 9.7% (n = 10). The inhibitions of membrane capacitance by Rb₁, Rc, Re, Rf, and Rg₁ were 35.3 ± 5.5% (n = 7); 41.8 ± 7.0% (n = 8); 40.5 ± 5.9% (n = 9); 51.2 ± 7.6% (n = 9); and 35.9 ± 5.1% (n = 10), respectively. The inhibitory potencies of the ginsenosides on ΔC_m were Rf > Rc > Re > Rg₁ > Rb₁. Therefore, we found that GTS and ginsenosides exerted inhibitory effects on both Ca²⁺ currents and ΔC_m in rat adrenal chromaffin cells. These results suggest that ginseng saponins regulate catecholamine secretion from adrenal chromaffin cells and this regulation could be the cellular basis of antistress effects induced by ginseng.     

~3H—人参皂甙单体Rg~1、Rb~1、Rb~2在小鼠体内分布的整体放射自显影研究

以~3H标记的人参皂甙单体R_(g1)、R_(b1)、R_(b2)为示踪剂分别在三只雄性昆明种小鼠中经灌胃或尾静脉注射给于500uci,2h后乙醚麻醉致死,进行整体切片自显影。结果表明,三种皂甙单体都有肝、肾、心、肺、脾、胃、肠、胆囊、膀胱分布;R_(g1)和R_(b1)还可通过血脑屏障进入脑组织,特别是R_(g1);R_(b1)在毛囊、肾上腺和眼内有明显分布;Rb_2在造血红骨髓(如脊柱)、毛囊、肾上腺中的分布有其特点,提示三种单体均有胆-肠和肾-膀胱排泄,Rb_1以后者为主。     

高效液相色谱法测定人参中多菌灵农药残留含量

 目的建立了测定中药材人参中多菌灵农药残留量方法。方法采用RP-HPLC法,Diamonsil C₁₈色谱柱。流动相为甲醇-四氢呋喃-水(43∶2∶55),检测波长为277 nm。结果平均回收率人参茎叶83.94%,RSD为2.42%(n=6);平均回收率人参根87.38%,RSD为2.68%(n=6)。多菌灵在1.926～192.6 ng时,r=1.000 0,呈良好的线性关系。结论本方法简便、快速、适合同类中药材中多菌灵农药残留量测定与安全监控。     

Beneficial effect of ginseng root in SOD-1 (G93A) transgenic mice

Many patients with amyotrophic lateral sclerosis (ALS; motor neuron disease) use natural or traditional therapies of unproven benefit. One such therapy is ginseng root. However, in some other disease models, ginseng has proven efficacious. Ginseng improves learning and memory in rats, and reduces neuronal death following transient cerebral ischemia. These effects of ginseng have been related to increases in the expression of nerve growth factor and its high affinity receptor in the rat brain, and antioxidant actions, inter alia. Since such actions could be beneficial in ALS as well, we studied the effect of ginseng (Panax quinquefolium), 40 and 80 mg/Kg, in B6SJL-TgN(SOD1-G93A)1Gur transgenic mice. The ginseng was given in drinking water, from age 30d onwards. We measured the time to onset of signs of motor impairment, and survival. There was no difference between the two ginseng groups (n=6, 6) in either measure. However, compared to controls (n=13), there was a prolongation in onset of signs (116d vs. 94d, P<0.001), and survival (139d vs. 132d, P<0.05). These experiments lend support to the use of ginseng root in ALS. Future experiments using this model could examine for symptomatic effects of ginseng, measure the effect of specific ginsenosides (which differ between ginseng species), and elucidate their mechanisms of action.