This study examined the laxative effects of hot-water extracts of Hovenia dulcis Thunb. (HD), Phyllostachys pubescens Mazel (PM), and a 2:8 mixture of both (HP) in two chronic constipation models. For the loperamide-induced constipation model, animals were divided into an untreated group, negative control group (loperamide 4 mg/kg), positive control group (bisacodyl 4 mg/kg) group, and six treatment groups (HP 100 or 400, HD 50 or 100, and PM 100 or 400 mg/kg). For the low-fiber diet-induced constipation model, animals were divided into an untreated group (normal diet), negative control group (low-fiber diet), positive control group (Agio granule, 620 mg/kg), and the same treatment groups. Fecal number, weight, fecal water content, and intestinal transit ratio were higher in the groups treated with HP, HD, and PM than in the groups treated with loperamide or low-fiber diet. Thickness of colon mucosa and muscle layers were increased in the treated groups. Colon tension increased in the HP groups, and [Ca2+]i measurements using fura-2 as an indicator showed that HP inhibits ATP-mediated Ca2+ influx in IEC-18 cells. These results showed that the HP mixture has laxative activity by increased mucin secretion and inducing contractile activity and relaxation. It may be a useful therapeutic strategy for ameliorating in chronic constipation.
Katsoulos, Panagiotis D.;Karatzia, Maria A.;Boscos, Constantinos;Wolf, Petra;Karatzias, Harilaos
Journal of Animal Science and Technology
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v.58
no.7
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pp.24.1-24.7
/
2016
Background: Clinoptilolite is a natural zeolite with high adsorption capacity for polar mycotoxins such as aflatoxins. The efficacy of clinoptilolite in ameliorating the toxic effects of aflatoxicosis has been proven in monogastric animals, but there is no such evidence for ruminants. The aim of this study was to evaluate, under field conditions, whether the dietary administration of clinoptilolite in dairy cows could reduce the concentration of aflatoxin M1 ($AFM_1$) in bulk-tank milk, in farms with higher than or close to $0.05{\mu}g/kg$ of milk (European maximum allowed residual level). An objective of the present study was also to investigate the effect of particle size of clinoptilolite on aflatoxin binding. Methods: Fifteen commercial Greek dairy herds with AFM1 concentrations in bulk tank milk ${\geq}0.05{\mu}g/kg$ were selected. Bulk tank milk AFM1 was determined prior to the onset and on day 7 of the experiment. Clinoptilolite was added in the total mixed rations of all farms at the rate of 200 g per animal per day, throughout this period. Two different particle sizes of clinoptilolite were used; less than 0.15 mm in 9 farms (LC group) and less than 0.8 mm in 6 farms (HC group). Results: Clinoptilolite administration significantly reduced $AFM_1$ concentrations in milk in all farms tested at an average rate of 56.2 % (SD: 15.11). The mean milk $AFM_1$ concentration recorded on Day 7 was significantly (P < 0.001) lower compared to that of Day 0 ($0.036{\pm}0.0061$ vs. $0.078{\pm}0.0074{\mu}g/kg$). In LC group farms the reduction of milk $AFM_1$ concentration was significantly higher than HC group farms ($0.046{\pm}0.0074$ vs. $0.036{\pm}0.0061{\mu}g/kg$, P = 0.002). As indicated by the Pearson correlation, there was a significant and strong linear correlation among the milk $AFM_1$ concentrations on Days 0 and 7 (R = 0.95, P < 0.001). Conclusions: Dietary administration of clinoptilolite, especially of smallest particle size, at the rate of 200 g per cow per day can effectively reduce milk $AFM_1$ concentration in dairy cattle and can be used as a preventive measure for the amelioration of the risks associated with the presence of aflatoxins in the milk of dairy cows.
${\alpha}$-Asarone exhibits a number of pharmacological actions including neuroprotective, anti-oxidative, anticonvulsive, and cognitive enhancing action. The present study investigated the effects of ${\alpha}$-asarone on pro-inflammatory cytokines mRNA, microglial activation, and neuronal damage in the hippocampus and on learning and memory deficits in systemic lipopolysaccharide (LPS)-treated C57BL/6 mice. Varying doses of ${\alpha}$-asarone was orally administered (7.5, 15, or 30 mg/kg) once a day for 3 days before the LPS (3 mg/kg) injection. ${\alpha}$-Asarone significantly reduced TNF-${\alpha}$ and IL-$1{\beta}$ mRNA at 4 and 24 hours after the LPS injection at dose of 30 mg/kg. At 24 hours after the LPS injection, the loss of CA1 neurons, the increase of TUNEL-labeled cells, and the up-regulation of BACE1 expression in the hippocampus were attenuated by 30 mg/kg of ${\alpha}$-asarone treatment. ${\alpha}$-Asarone significantly reduced Iba1 protein expression in the hippocampal tissue at a dose of 30 mg/kg. ${\alpha}$-Asarone did not reduce the number of Iba1-expressing microglia on immunohistochemistry but the average cell size and percentage areas of Iba1-expressing microglia in the hippocampus were significantly decreased by 30 mg/kg of ${\alpha}$-asarone treatment. In the Morris water maze test, ${\alpha}$-asarone significantly prolonged the swimming time spent in the target and peri-target zones. ${\alpha}$-Asarone also significantly increased the number of target heading and memory score in the Morris water maze. The results suggest that inhibition of pro-inflammatory cytokines and microglial activation in the hippocampus by ${\alpha}$-asarone may be one of the mechanisms for the ${\alpha}$-asarone-mediated ameliorating effect on memory deficits.
Objectives: TuRo, defined as a dance therapy applying the meridian Qi system into the dancing movements, may have effects on ameliorating the psychological symptoms that often appear in adolescent students in a stressful situation. The Objective of the present study was to examine whether TuRo training relieves the psychological symptoms in adolescent female students. Methods: Symptom Check List-90-Revision (SCL-90-R), a 5 point Likert scale, consisted of 90 items that represent psychological symptoms, were used to measure the psychological health status in healthy adolescent female. Twenty two adolescent female students were trained TuRo dancing for two months while 29 in control group were trained mimicked movements without the concept of Qi for the same period. Changes in Somatization, Obsessive-Compulsive behaviors, Interpersonal Sensitivity, Depression, Anxiety, Hostility, Phobic Anxiety, Parinoid Ideation and Psychotic symptoms by the two months of training were compared between TuRo and control groups using SCL-9Q-R. Results: Among the nine-categorized psychological symptoms, the somatization and hostility were significantly reduced in TuRo group (p
The effects of the oriental herbal medicine Saenghyetang(SHT, 生慧湯), which consists of Rehmanniae Radix (熟地黃 九蒸: was made by 9th steam) 40g, Corni Fructus(山茱黃) 16g, Polygalae Radix(遠志) 8g, Zizyphi Spinosae Semen(酸棗仁) 2g, Biotae Semen(柏子仁 去油: oil ingredient was removed) 20g, Poria Cocos(茯笭) 12g, Ginseng Radix(人蔘) 12g, Acori Graminei Rhizoma(石菖蒲) 2g, Sinapis Semen(白芥子) 8g, on learning ability and memory were investigated. Hot water extract(HWE) and ethanol extract(EE) from SHT were used for the studies. Learning ability and memory are related to modifications of synaptic strength among neurons that interactive. Enhanced synaptic coincidence detection leads to improved learning ability and memory. If the NMDA receptor, a synaptic coincidence detector, acts as a graded switch for memory formations, enhanced signal detection by NMDA receptors should enhance learning ability and memory. It was shown that NR2B was increased in the forebrains of oriental medicine-administrated mice, leading to enhanced activation of NMDA receptors and facilitating synaptic potentiation in response to stimulation at 10-100 Hz. These HWE-SHT treated mice exhibited that superior ability in learning and memory when performing various behavioral tasks, showing that NR2B is enhanced by HWE-SHT treatment and also is critical in gating the age-dependent threshold for plasticity and memory formation. NMDA receptor-dependent modifications, which were mediated in part by HWE administration, of synaptic efficacy, therefore, represent a mechanism for associative learning ability and memory. Results suggest that oriental medical enhancement of NR2B contributes to increase intelligence and memory in mammals On the other hand, to examine the effects of EE-SHT on the learning ability and memory in experimental mice, EE-SHT was tested on passive and active avoidance responses. The EE-SHT ameliorated the memory retrieval deficit induced by ethanol in mice, but not other memory impairments. EE-SHT(10, 20mg/100 g, p.o.) did not affect the passive avoidance responses of normal mice in the step through and step down tests, the conditioned and unconditioned avoidance responses of normal mice in the shuttle box, lever press performance tests and the ambulatory activity of normal mice in a normal condition. However, EE-SHT at 20 mg/kg significantly decrease the spontaneous motor activity during the shuttle box test, and also to extend the sleeping time induced by pentobarbital in mice. These results suggest that SHT has an ameliorating effect on memory retrieval impairments and a weak tranquilizing action.
Objective: This pilot study was performed to investigate the effect of metformin on insulin resistance, hormone levels, and lipid profiles in non-obese patients with polycystic ovary syndrome. Methods: This study included 16 non-obese patients with polycystic ovary syndrome diagnosed at our hospital from June 2006 to September 2007. Blood samples were collected before and 6 months after metformin treatment for analysis of fasting serum glucose levels, fasting serum insulin levels, a glycemic response to 75 g oral glucose tolerance test (OGTT), and hormonal blood profile including FSH, LH, estradiol, testosterone, free testosterone, serum lipid profiles. Insulin resistance was estimated by calculating fasting glucose/insulin ratio (FGIR), 2 hr glucose/insulin ratio after 75 g glucose load. And we investigated insulin resistance and pancreatic beta cell function by calculating HOMA beta cell function and HOMA IR. Results: After the treatment of metformin, there was significant increase in 2 hr glucose/insulin ratio after 75 g glucose load (p=0.04) and decrease in HOMA IR (p=0.000). But serum lipid profiles did not change significantly. Also the metformin treatment induced a significant reduction in serum free testosterone and LH levels, and LH/FSH ratio (p=0.001, p=0.000, p=0.034). Conclusion: This pilot study showed that metformin might be effective in improving insulin sensitivity, ameliorating hyperandrogenemia in non-obese patients with polycystic ovary syndrome. Further investigations with larger number of patients and long-term observations are necessary to determine the role of metformin.
Pena, Ike Dela;Yoon, Seo Young;Kim, Hee Jin;Park, Sejin;Hong, Eun Young;Ryu, Jong Hoon;Park, Il Ho;Cheong, Jae Hoon
Journal of Ginseng Research
/
v.38
no.1
/
pp.1-7
/
2014
Background: Although ginsenosides such as Rg1, Rb1 and Rg3 have shown promise as potential nutraceuticals for cognitive impairment, their use has been limited due to high production cost and low potency. In particular, the process of extracting pure Rg3 from ginseng is laborious and expensive. Methods: We described the methods in preparing ginseol k-g3, an Rg3-enriched fraction, and evaluated its effects on scopolamine-induced memory impairment in mice. Results: Ginseol k-g3 (25-200 mg/kg) significantly reversed scopolamine-induced cognitive impairment in the passive avoidance, but not in Y-maze testing. Ginseol k-g3 (50 and 200 mg/kg) improved escape latency in training trials and increased swimming times within the target zone of the Morris water maze. The effect of ginseol k-g3 on the water maze task was more potent than that of Rg3 or Red ginseng. Acute or subchronic (6 d) treatment of ginseol k-g3 did not alter normal locomotor activity of mice in an open field. Ginseol k-g3 did not inhibit acetylcholinesterase activity, unlike donezepil, an acetylcholinesterase inhibitor. Rg3 enrichment through the ginseol k-g3 fraction enhanced the efficacy of Rg3 in scopolamine-induced memory impairment in mice as demonstrated in the Morris water maze task. Conclusion: The effects of ginseol k-g3 in ameliorating scopolamine-induced memory impairment in the passive avoidance and Morris water maze tests indicate its specific influence on reference or long-term memory. The mechanism underlying the reversal of scopolamine-induced amnesia by ginseol k-g3 is not yet known, but is not related to anticholinesterase-like activity.
Background: This study was designed to investigate whether ginsenoside Rb1 (Rb1) and compound K (CK) ameliorated insulin resistance by suppressing endoplasmic reticulum (ER) stress-induced inflammation in adipose tissue. Methods: To induce ER stress, epididymal adipose tissue from mice or differentiated 3T3 adipocytes were exposed to high glucose. The effects of Rb1 and CK on reactive oxygen species production, ER stress, TXNIP/NLRP3 inflammasome activation, inflammation, insulin signaling activation, and glucose uptake were detected by western blot, emzyme-linked immunosorbent assay, or fluorometry. Results: Rb1 and CK suppressed ER stress by dephosphorylation of $IRE1{\alpha}$ and PERK, thereby reducing TXNIP-associated NLRP3 inflammasome activation in adipose tissue. As a result, Rb1 and CK inhibited IL-$1{\beta}$ maturation and downstream inflammatory factor IL-6 secretion. Inflammatory molecules induced insulin resistance by upregulating phosphorylation of insulin receptor substrate-1 at serine residues and impairing insulin PI3K/Akt signaling, leading to decreased glucose uptake by adipocytes. Rb1 and CK reversed these changes by inhibiting ER stress-induced inflammation and ameliorating insulin resistance, thereby improving the insulin IRS-1/PI3K/Akt-signaling pathway in adipose tissue. Conclusion: Rb1 and CK inhibited inflammation and improved insulin signaling in adipose tissue by suppressing ER stress-associated NLRP3 inflammation activation. These findings offered novel insight into the mechanism by which Rb1 and CK ameliorate insulin resistance in adipose tissue.
Zhong, Yong-Mei;Hisao Nishijo;Teruko Uwano;Hidetishi Yamaguchi;Taketosho Ono
Proceedings of the Ginseng society Conference
/
1998.06a
/
pp.1-11
/
1998
Ameliorating mechanisms of red ginseng on learning deficits were investigated in the following 3 experiments; its effects on 1) place learning deficits in aged rats and in young rats with selective hippocampal lesions (behavioral study), 2) long-term potentiation in the hippocampal formation (neuro- physiological study), and 3) ChAT (choline acetyl transferase) activity in various brain regions of aged rats (pharmacological study). In the behavioral study, first, performance in the place learning tasks were compared among 3 groups of young and aged rats; control young intact rats (10-12 week old) treated with water, aged rats (28-32 month old) treated with water, and aged rats (28-32 month old) treated with red ginseng (100 mghglday) suspended in water. Second, performance in the place learning tasks was compared among 3 groups of young rats; control intact rats treated with water, rats with bilateral hippocampal lesions treated with water, and rats with bilateral hippocampal lesions treated with red ginseng (100 mg/kg/day). Each rat in these 2 behavioral experiments was tested with the 3 types of the place learning tasks in a circular open field using intracranial self-stimulation (ICSS) as reward. The ICSS reward was delivered if the rat (1) moved distance of 100-160 cm (DMT): (2) entered an experiment-determined reward place within the open field, and this place was randomly varied in sequential trials (RRPST); or (3) entered 2 specific places, and did a shuttle behavior between the 2 places (PLT). Performance of the aged rats in the ginseng group was not significantly different from that of control young rats in ICSS (current intensity, bar press rates), DMT and RRPST. However, treatment with red ginseng significantly ameliorated place-navigation learning deficits in aged rats in the PLT. Similarly, red ginseng ameliorated learning and memory deficits in young rats with hippocampal lesions in the same tasks. In the neurophysiological study using young rats, perfusion of hippocampal slices with non-sapon in fraction of red ginseng significantly enhanced magnitudes of the long-term potentiation (LfP) in the CA3 subfield. In the pharmacological study, treatment with red ginseng did not affect ChAT activity in aged rat brain including the hippocampal formation. These results strongly suggest that red ginseng ameliorates learning and memory deficits in aged rats through actions on the CA3 subfield of the hippocampal formation, which were independent of the presynaptic components of the cholinergic system
Kim, Hyeon-Joong;Jung, Seok-Won;Kim, Seog-Young;Cho, Ik-Hyun;Kim, Hyoung-Chun;Rhim, Hyewhon;Kim, Manho;Nah, Seung-Yeol
Journal of Ginseng Research
/
v.42
no.4
/
pp.401-411
/
2018
Longevity in medicine can be defined as a long life without mental or physical deficits. This can be prevented by Alzheimer's disease (AD). Current conventional AD treatments only alleviate the symptoms without reversing AD progression. Recent studies demonstrated that Panax ginseng extract improves AD symptoms in patients with AD, and the two main components of ginseng might contribute to AD amelioration. Ginsenosides show various AD-related neuroprotective effects. Gintonin is a newly identified ginseng constituent that contains lysophosphatidic acids and attenuates AD-related brain neuropathies. Ginsenosides decrease amyloid ${\beta}$-protein ($A{\beta}$) formation by inhibiting ${\beta}$- and ${\gamma}$-secretase activity or by activating the nonamyloidogenic pathway, inhibit acetylcholinesterase activity and $A{\beta}$-induced neurotoxicity, and decrease $A{\beta}$-induced production of reactive oxygen species and neuro-inflammatory reactions. Oral administration of ginsenosides increases the expression levels of enzymes involved in acetylcholine synthesis in the brain and alleviates $A{\beta}$-induced cholinergic deficits in AD models. Similarly, gintonin inhibits $A{\beta}$-induced neurotoxicity and activates the nonamyloidogenic pathway to reduce $A{\beta}$ formation and to increase acetylcholine and choline acetyltransferase expression in the brain through lysophosphatidic acid receptors. Oral administration of gintonin attenuates brain amyloid plaque deposits, boosting hippocampal cholinergic systems and neurogenesis, thereby ameliorating learning and memory impairments. It also improves cognitive functions in patients with AD. Ginsenosides and gintonin attenuate AD-related neuropathology through multiple routes. This review focuses research demonstrating that ginseng constituents could be a candidate as an adjuvant for AD treatment. However, clinical investigations including efficacy and tolerability analyses may be necessary for the clinical acceptance of ginseng components in combination with conventional AD drugs.
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