• 대한한의학회지
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• 제27권2호
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• pp.253-261
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• 2006

Backgrounds : Hyperlipidemia is a major cause of cardiovascular disease (CVD). Lowering serum cholesterol levels could reduce the risk of CVD. Insamsansa-eum (Renshenshanzha-yin, ISE), composed of Ginseng Radix and Crataegii Fructus, is a new medicine developed to treat hyperlipidemia and CVD. Objectives : In this study, we intended to explore the clinical effects of ISE on patients with hypercholesterolemia, and moreover we also compared its effects according to the pattern identification. Methods : Subjects were administered ISE with the dose of 600 mg three times a day for 4 weeks. Patterns of subjects were identified with diagnostic scoring system for Yin-Yang and the condition of Excess-Deficiency before treatment. Serum lipids were measured at baseline and after 4 weeks of medication. Results : ISE lowered total cholesterol(TC), triglyceride(TG), total lipid(TL), phospholipid(PL) and low density lipoprotein cholesterol(LDL) significantly. Compared with the data of our previous study, it was less effective than Atorvastatin but showed equal lipids-lowering effect to Chunghyul-dan (Qingxue-dan, CHD). In Yang pattern group, ISE was less effective in lowering TG and LDL than it was in not-Yang-not-Yinpattern group. On safety assessment, there was no adverse effect, hepatic or renal toxicity. Conclusions : We suggest that ISE is a safe and useful herbal medicine for hypercholesterolemia, and moreover it could be more useful when it is used for patients with not Yang pattern.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.194-199
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• 2002

Many oxidative metabolites of tetrahydrocannabinols (THCs), active components of marijuana, were pharmacologically active, and 11-hydroxy-THCs, 11-oxo-${\Delta}^8$-THC, 7-oxo-${\Delta}^8$-THC, 8$\beta$, 9$\beta$-epoxyhexahydrocannabinol (EHHC), 9$\alpha$, l0$\alpha$-EHHC and 3'-hydroxy-${\Delta}^9$-THC were more active than THC in pharmacological effects such as catalepsy, hypothermia and barbiturate synergism in mice. Cannabidiol (CBD), another major component, was biotransfomred to two novel metabolites, 6-hydroxymethyl-${\Delta}^9$-THC and 3-pentyl-6, 7, 7a, 8, 9, lla-hexahydro-I, 7-dihydroxy-7, 1O-dimethyldibenzo[b, d]oxepin (PHDO) through 8R, 9-epoxy-CBD and 85, 9-epoxy-CBD, respectively. Both metabolites exhibited some pharmacological effects comparable to d9 - THe. Cannabinol (CBN), the other major component, was mainly metabolized to ll-hydroxy-CBN by hepatic microsomes of animals including humans. The pharmacological effects of the metabolite were higher than those of CBN demonstrating that II-hydroxylation of CBN is metabolic activation pathway of the cannabinoid as is the case in THCs. Tolerance and reciprocal cross-tolerance developed to pharmacological effects d8 - THC and ll-hydroxy-d8-THC , and the magnitude of tolerance development produced by the metabolite was significantly higher than that by d8-THC. The results indicate that ll-hydroxy-d8-THC has an important role not only in the pharmacological effects but also its tolerance development of d8 - THe. THCs and their metabolites competed to the specific binding of CP-55, 940, an agonist of cannabinoid receptor, to synaptic membrane from bovine cerebral cortex. The Ki value of THCs and their metabolites were closely paralleled to their pharmacological effects in mice. A novel cytochrome P450 (cyp2c29) was purified and identified as a major enzyme responsible for the metabolic activation of d8-THC at the II-position in the mouse liver. cDNA of CYP2C29 was cloned from a mouse cDNA library and its sequence was determined. The oxidation mechanism of THC by cyp2c29 was proposed.

• 대한수의학회지
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• 제16권1호
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• pp.59-64
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• 1976

In the sequence of carbon tetrachloride hepatotoxicity, increased serum levels of a number of enzymes have been demonstrated in experimental animals. These observations, therefore, have served to help in detecting hepatic injury. The serological influence of chlorpromazine (CPZ) and iproniazid on the acute $CCl_4$ poisoning was executed in this investigation taking use of 6 albino rabbits (around 2 kg b.w.) in each group. By measuring of blood sugar level (Nelson-Somogyi method), S-GOT and S-GPT activities (Reitman-Frankel method), the pharmacological effects of the drugs was evaluated setting pretreated groups against the control. The results obtained were summarized as follows: 1. The intramuscular injection of $CCl_4$ led to increase the blood sugar level in first 3 hours and, after that, to decrease reasonably. But CPZ-pretreated group showed a tendency of increasing in compare with the control, and iproniazid-pretreated group inhibited evidently. 2. In S-GOT activity, the increased level was induced by $CCl_4$ in control. And CPZ-pretreated group showed a increased level until first day and decreased rapidly. But this property inhibited inhibited significantly by pretreating with iproniazid. 3. Although a single dose of $CCl_4$ increased the S-GPT activity, the more increasing trend was observed in CPZ-pretreated group. But these tendencies depressed remarkably in the iproniazid-pretreated group. It seemed to be attributed not to defend the $CCl_4$ toxicity but to be suppressed the enzyme systems in the liver by iproniazid that the blood sugar level and serum transaminase activities was decreased significantly in pretreating with iproniazid.

• 대한임상독성학회지
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• 제13권2호
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• pp.71-77
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• 2015

Purpose: Acute endosulfan poisoning is rare but causes significant morbidity and mortality. The aim of our study is to describe complications and features of seizure and determine factors associated with mortality in acute endosulfan poisoning. Methods: Twenty-eight adult patients with acute endosulfan poisoning admitted to our emergency department during a 15-year period were studied retrospectively. The clinical features of seizure, use of antiepileptic drugs during seizure, and hospital courses were evaluated. Clinical factors between survived group and non-survived group were compared for identification of factors associated with mortality. Results: Of the 28 patients with endosulfan poisoning, 4 patients (14.3%) died and 15 (53.6%) patients developed generalized tonic-clonic seizure. Thirteen patients (46.4%) and 5 patients (17.9%) progressed to status epilepticus (SE) and refractory status epilepticus (RSE), respectively. SE and RSE were associated with mortality. Almost all significant complications including shock, acute renal failure, hepatic toxicity, rhabdomyolysis, and cardiac injury developed in SE and RSE patients. Conclusion: SE and RSE were important contributors to death in endosulfan poisoning. Emergency physicians treating endosulfan poisoning should make an effort not to progress seizure following endosulfan poisoning to SE and RSE using a rapid and aggressive antiepileptic drug.

• 대한임상독성학회지
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• 제10권2호
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• pp.91-96
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• 2012

Purpose: A retrospective study with a literature review was conducted to identify the clinical characteristics and prognosis after the acute ingestion of glacial acetic acid. Methods: The medical records of 20 patients,who had presented to the emergency department of Ajou University Hospital complaining of the acute ingestion of glacial acetic acid between January 2006 and December 2011, were examined retrospectively. Results: Among the 172 patients admitted for caustics injury, 20 patients ingested glacial acetic acid. The mean age of the patients was $55{\pm}23.5$, and the mean volume of the acid was $84.5{\pm}71.3$ ml. The clinical features included 1) oral ulcers in 12 patients (63.2%), 2) respiratory difficulties in 11 patients (57.9%), 3) oliguria in 8 patients (42.1%), 4) renal toxicity in 7 patients (36.8%), 5) hepatic failure in 7 patients (36.8%), 6) disseminated intravascular boagulopathyin 7 patients (36.8%), 7) low blood pressure in 8 patients (42.1%), and 8) mental changes in 9 patients (47.4%). Ten patients required endotracheal intubation. Nine patients were admitted to the intensive care unit, and 5 patients expired. Conclusion: The ingestion of glacial acetic acid can cause severe symptoms, such as metabolic acidosis, multiple organ failure and upper airway swelling frequently and has a high mortality rate. Therefore, aggressive treatment, including endotracheal intubation, should be considered at the early stages.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제11권sup1호
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• pp.72-82
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• 2008

Wilson disease (WD) is an autosomal recessive disorder of copper metabolism that results in accumulation of copper primarily in the liver, the brain and the cornea. Mutations in the WD gene, ATP7B cause failure of copper excretion from hepatocyte into bile and a defective synthesis of ceruloplasmin. More than 370 mutations are now recognized, scattering throughout the ATP7B gene. Since WD has protean clinical presentations, awareness of WD in clinical practice is important for the early diagnosis and prevention of accumulated copper toxicity. None of the laboratory parameters alone allows a definite diagnosis of WD. There are numerous pitfalls in the diagnosis of WD. Low serum ceruloplasmin concentrations, increased 24 hour urinary copper excretion, increased hepatic copper concentrations and the presence of Kayser-Fleischer rings in the cornea are major diagnostic points. A combination of any two of these 4 laboratory findings is strong support for a diagnosis of WD. Molecular methods are now being used to aid diagnosis. Molecular genetic testing has confirmed the diagnosis in individuals in whom the diagnosis is not clearly established biochemically and clinically. Siblings should be screened for WD once an index case has been diagnosed. Discrimination of heterozygotes from asymptomatic patients is essential to avoid inappropriate lifelong therapy for heterozygotes. Genetic testing, either by haplotype analysis or by mutation analysis, is the only reliable tool for differentiating heterozygote carriers from affected asymptomatic patients. Currently, genetic testing is of limited value in the primary diagnosis. However, genetic testing will soon play an essential role in diagnosing WD as rapid advancement of biomedical technology will allow more rapid, easier and less expensive mutation detection.

• Asian Pacific Journal of Cancer Prevention
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• 제16권15호
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• pp.6595-6597
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• 2015

Objective: To investigate short- and long-term treatment effects and side reactions of lobaplatin plus 5-Fu combined and concurrent radiotherapy in treating patients with inoperable middle-advanced stage esophageal cancer. Methods: Sixty patients with middle-advanced stage esophageal squamous cell cancer were retrospectively analyzed. All patients were administered lobaplatin (50 mg intravenously) for 2 h on day 1, and 5-Fu ($500mg/m^2$) injected intravenously from day 1 to 5 for 1 cycle, in an interval of 21 days for totally 4 cycles. At the same time, late-course accelerated hyperfractionated three-dimensional conformal radiotherapy was performed. Patients were firstly treated with conventional fractionated irradiation (1.8 Gy/d, 5 times/week, a total of 23 treatments, and DT41.4 Gy), and then treated with accelerated hyperfractionated irradiation (1.5 Gy, 2 times/d, a total of 27 Gy in 9 days, an entire course of 6-7 weeks, and DT 68.4Gy). Results: All patients completed treatment, including 10 complete response (CR), 41 partial response (PR), 7 stable disease (SD), and 2 progressive disease (PD). The total effective rate was 85.0% (51/60). Thirty-nine patients had an increased KPS score. One-, 2-, and 3-year survival rates were 85.3%, 57.5%, and 41.7%, respectively. The median survival time was 27 months. The adverse reactions included myelosuppression, which was mainly degree I and II. The occurrence rate of radiation esophagitis was 17.5%. No significant hepatic or renal toxicity was observed. Conclusion: Lobaplatin plus 5-Fu combined with concurrent radiotherapy is safe and effective in treating patients with middle-advanced stage esophageal cancer. However, this result warrants further evaluation by randomized clinical studies.

• 사상체질의학회지
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• 제21권3호
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• pp.209-215
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• 2009

1. Objects: This case study reports a liver injury in treatment of constipation with Yeoldahanso-tang plus Rheum rhabarbarum. 2. Methods: The patient's subjective symptoms and the laboratory data including aspartate transaminase(AST), alanine transaminase(ALT), alkaline phosphatase(ALP), and gamma($\gamma$)-glutamyl transpeptidase(GGT) were observed before and after liver injury. We used the Roussel Uclaf Causality Assessment Method(RUCAM) scale in order to find out whether if Yeoldahanso-tang plus Rheum rhabarbarum was related with the liver injury. 3. Results: The patient's AST and ALT were elevated more than twice after a 3week administration period of herbal medicine. After discontinuation of the herbal medicine and administration of hepatic protective medication, AST and ALT decreased. The patient's general condition improved during hospitalization. The RUCAM score was estimated at 8. 4. Conclusions: This case is presented to bring more attention to the toxicity of herbal medicine.

• Archives of Pharmacal Research
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• 제28권9호
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• pp.995-1001
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• 2005

Morphine-induced analgesia has been shown to be antagonized by ginseng total saponins (GTS), which also inhibit the development of analgesic tolerance to and physical dependence on morphine. GTS is involved in both of these processes by inhibiting morphine-6-dehydrogenase, which catalyzes the synthesis of morphinone from morphine, and by increasing the level of hepatic glutathione, which participates in the toxicity response. Thus, the dual actions of ginseng are associated with the detoxification of morphine. In addition, the inhibitory or facilitated effects of GTS on electrically evoked contractions in guinea pig ileum (I-L-receptors) and mouse vas deferens $(\delta-receptors)$ are not mediated through opioid receptors, suggesting the involvement of non-opioid mechanisms. GTS also attenuates hyperactivity, reverse tolerance (behavioral sensitization), and conditioned place preference induced by psychotropic agents, such as methamphetamine, cocaine, and morphine. These effects of GTS may be attributed to complex pharmacological actions between dopamine receptors and a serotonergic/adenosine $A_{2A}1\delta-opioid$ receptor complex. Ginsenosides also attenuate the morphine-induced cAMP signaling pathway. Together, the results suggest that GTS may be useful in the prevention and therapy of the behavioral side effects induced by psychotropic agents.

• 한국환경보건학회지
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• 제12권2호
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• pp.1-9
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• 1986

The purpose of this study is to determine the antidotal effects of thiamine in phenylmercury poisoning rats. Sixty-six rats were divided into six groups the control group, the $40{\gamma}$ thiamine-only-dosed group, the 6 ppm phenylmercury-only-dosed group, the simultaneously-dosed-group with 6 ppm mercury & $20{\gamma}$ thiamine, and with 6 ppm mercury & $40{\gamma}$ thiamine, and with 6 ppm mercury & $80{\gamma}$ thiamine. The thiamine was put into pellet by various concentrations, and phenylmercury was mixed in drinking water by 6 ppm concentration. The rats were sacrificed for observing the histopathological changes of brain, liver and kidney. The remits summarized are as follows 1. In the group dosed with only $40{\gamma}$ thiamine, the tissues of brain, liver and kidney did not show any abnormal architecture. 2. The phenyhnercury-only-dosed group and the simultaneoulsy-dosed group with mercury and $20{\gamma}$ thiamine showed remarkable degenerative or necrotic hepatic cells. In addition, a remarkable swelling and necrosis on epithelium of proximal tubules in kidney were found. 3. The simultaneously-dosed group with mercury and $40{\gamma}$ thiamine showed moderate degeneration and necrosis of Purkinje cells in cerebellum. A moderate necrosis and swelling on epithelium of proximal tubules and a large amount of tubular casts were found as well. 4. The simultaneously-dosed group with mercury and $80{\gamma}$ thiamine showed a slight degenerative change of Purkinje cells. A slight degenerative change on epithelium of proximal tubules and a small amount of tubular casts were also found.