• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.2
• /
• pp.261-269
• /
• 1998

Concomitant administration of a single acute dose of ethanol (4 g/kg) protected mice from the hepatocellular injury observed upon administration of a large dose of acetaminophen (400 mg/kg). This was evidenced by the normal histological appearances of liver sections and by the lowered serum aminotransferase activities in mice treated with ethanol and acetaminophen together. In the mice treated with acetaminophen alone, along with the hepatic necrosis, the hepatic microsomal aminopyrine N-demethylase activity was decreased. However, co-administration of ethanol prevented this acetaminophen dependent inhibition on the microsomal mixed function oxidase activity. Pharmacokinetic studies indicated that the concentration of un-metabolized drug in the blood was increased in the ethanol treated mice. Furthermore, upon co-administration of ethanol, although the biliary levels of acetaminophen metabolites (glucuronide, sulfate and cysteine conjugates) were decreased, the level of unmetabolized acetaminophen was increased. Our findings suggest that co-administration of an acute dose of ethanol reduces the degree of hepatocellular necrosis produced by a large dose of acetaminophen and this ethanol dependent protection is, in major part, afforded by suppression of the hepatic microsomal mixed function oxidase activity catalyzing the metabolic activation of acetaminophen.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.18 no.4
• /
• pp.957-964
• /
• 2004

Herbal medicines are increasingly used to treat various diseases and lots of studies have been reported that they had benefits in treating and preventing of diseases. But organic toxicity is increasingly recognized as herbal medicines become more popular in industrialized countries. Some herbal products potentially benefit people with lots of diseases, however these benefits remain generally unproved in humans, and a greater awareness for potential adverse effects is required. A herb containing a wide variety of, mostly unknown, substances may well include some with unwanted effects. This review focuses on emerging organic toxicities that have been observed associated with various herbal preparations involving the liver, kidney, and heart, and patterns of organ injury, potential risk factors for organic toxicities. In addition to the potential for organic toxicities, drug drug interactions between herbal medicines and conventional agents may affect the efficacy and safety of concurrent medical therapy. Appropriate reporting and regulatory system to monitor herbal toxicity are required, in conjunction with ongoing scientific evaluation of the potential benefits of phytotherapy.

• The Korean Journal of Physiology and Pharmacology
• /
• v.3 no.6
• /
• pp.579-586
• /
• 1999

Complement-mediated neutrophil activation has been hypothesized to be an important mechanism of reperfusion injury. It has been proposed that C1 esterase inhibitor (C1 INH) may prevent the complement- dependent activation of polymorphonuclear leukocytes (PMNs) that occurs within postischemic myocardium. Therefore, The effect of C1 INH was examined in neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of C1 INH (5 mg/Kg) to I/R hearts in the presence of PMNs $(100{\times}10^6)$ and homologous plasma improved coronary flow and preserved cardiac contractile function (p＜0.001) in comparison to those I/R hearts receiving only vehicle. In addition, C1 INH significantly (p＜0.001) reduced PMN accumulation in the ischemic myocardium as evidenced by an attenuation in myeloperoxidase activity. These findings demonstrate the C1 INH is a potent and effective cardioprotective agent inhibits leukocyte-endothelial interaction and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.

• The Korean Journal of Physiology and Pharmacology
• /
• v.13 no.4
• /
• pp.295-300
• /
• 2009

It was evaluated the inhibitory action of quercetin-3-O-${\beta}$-D-glucuronopyranoside (QGC) on reflux esophagitis and gastritis in rats. QGC was isolated from the herba of Rumex Aquaticus. Reflux esophagitis or gastritis was induced surgically or by administering indomethacin, respectively. Oral QGC decreased ulcer index, injury area, gastric volume, and acid output and increased gastric pH as compared with quercetin. Furthermore, QGC significantly decreased gastric lesion sizes induced by exposing the gastric mucosa to indomethacin. Malondialdehyde levels were found to increase significantly after inducing reflux esophagitis, and were reduced by QGC, but not by quercetin or omeprazole. These results show that QGC can inhibit reflux esophagitis and gastritis in rats.

• The Korean Journal of Physiology and Pharmacology
• /
• v.4 no.5
• /
• pp.347-353
• /
• 2000

It has been well documented that a massive release of not only glutamate but also other neurotransmitters may modulate the final responses of nerve cells to the ischemic neuronal injury. But there is no information regarding whether the release of monoamines is directly associated with synaptic vesicular proteins under ischemia. In the present study, it was investigated whether synapsin 1, syntaxin and SNAP-25 are involved in the release of 5-hydroxytryptamine $([^3H]5-HT)$ in glucose/oxygen deprived (GOD) rat hippocampal slices. And, the effect of NMDA receptor using DL-2-amino-5-phosphonovaleric acid (APV) on ischemia- induced release of 5-HT and the changes of the above proteins were also investigated. GOD for 20 minutes enhanced release of $[^3H]5-HT,$ which was in part blocked by the NMDA receptor antagonist, APV. The augmented expression of synapsin 1 during GOD for 20 minutes, which was also in part prevented by APV. In contrast, the expression of syntaxin and SNAP-25 were not altered during GOD. These results suggest that ischemic insult induces release of $[^3H]5-HT$ associated with synapsin 1, synaptic vesicular protein, via activation of NMDA receptor in part.

• The Korean Journal of Physiology and Pharmacology
• /
• v.17 no.1
• /
• pp.81-87
• /
• 2013

Quercetin-3-O-${\beta}$-D-glucuronopyranoside (QGC) is a flavonoid glucoside extracted from Rumex Aquaticus Herba. In the present study, anti-oxidative and anti-inflammatory effects of QGC were tested in vitro. Epithelial cells obtained from cat esophagus were cultured. When the cells were exposed to acid for 2 h, cell viability was decreased to 36%. Pretreatment with 50 ${\mu}M$ QGC for 2 h prevented the reduction in cell viability. QGC also inhibited the productions of intracellular ROS by inflammatory inducers such as acid, lipopolysaccharide, indomethacin and ethanol. QGC significantly increased the activities of superoxide dismutase (SOD) and catalase, and also induced the expression of SOD2, while it restored the decrease of catalase expression in cells exposed to acid. QGC inhibited NF-${\kappa}B$ translocation, cyclooxygenase-2 expression and $PGE_2$ secretion in cells exposed to acid, which plays an important role in the pathogenesis of esophagitis. The data suggest that QGC may well be one of the promising substances to attenuate oxidative epithelial cell injury and inflammatory signaling in esophagus inflammation.

• The Korean Journal of Physiology and Pharmacology
• /
• v.22 no.2
• /
• pp.193-201
• /
• 2018

Connective tissue growth factor (CTGF) is a novel fibrotic mediator, which is considered to mediate fibrosis through extracellular matrix (ECM) synthesis in diabetic cardiovascular complications. Statins have significant immunomodulatory effects and reduce vascular injury. We therefore examined whether fluvastatin has anti-fibrotic effects in vascular smooth muscle cells (VSMCs) and elucidated its putative transduction signals. We show that advanced glycation end products (AGEs) stimulated CTGF mRNA and protein expression in a time-dependent manner. AGE-induced CTGF expression was mediated via ERK1/2, JNK, and Egr-1 pathways, but not p38; consequently, cell proliferation and migration and ECM accumulation were regulated by CTGF signaling pathway. AGE-stimulated VSMC proliferation, migration, and ECM accumulation were blocked by fluvastatin. However, the inhibitory effect of fluvastatin was restored by administration of CTGF recombinant protein. AGE-induced VSMC proliferation was dependent on cell cycle arrest, thereby increasing G1/G0 phase. Fluvastatin repressed cell cycle regulatory genes cyclin D1 and Cdk4 and augmented cyclin-dependent kinase inhibitors p27 and p21 in AGE-induced VSMCs. Taken together, fluvastatin suppressed AGE-induced VSMC proliferation, migration, and ECM accumulation by targeting CTGF signaling mechanism. These findings might be evidence for CTGF as a potential therapeutic target in diabetic vasculature complication.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.23 no.4
• /
• pp.895-897
• /
• 2009

Lonicera japonica has been widely used for chronic inflammatory diseases in many Asian countries. Its analgesic effect has not been explored yet. This study aimed to test the analgesic potential of methanol extracts from Lonicera japonica (MELJ) in rat neuropathic mctel. Neuropathic pain was pacts ed by partial sciatic nerve injury. Two weeks after surgery, neuropathic rats received oral administration of MELJ at doses of either 0.0 g/kg, 0.2 g/kg or 0.4 g/kg. At dose of 0.0 g, rats were administered with saline only and used as conracl. The behavioral tests for f 0.0 g, raand ccld hs were adma were weformed up to 2 hours after treatment. The MELJ at the dose 0.4 g/kg dmg gfg, ntly alleviated f 0.0 g, rahyperalgesia, but not cold hyperalgesia. These results showed that the MELJ had, although transient, analgesic effect on mechanical hyperalgesia in the rat neuropathic model.

• Journal of Sericultural and Entomological Science
• /
• v.2
• /
• pp.33-39
• /
• 1962

The results for the investigation of the various aromatic plants applied diets on silkworm raising from spring to autumn crops are found as followings. 1. There was no difference between the chemical menthol solution (1.0%) enriched diet and the normal diet for silkworm physiology. Neither injury nor advantage was obtained from the investigation. 2. It was found that there was no danger to use the mulberry leaves as silkworm diet by planting Mentha arvensis L. in the vacansy of mulberry farm, and no worse effect was found by rubbing the leaves of Mentha arvensis L. to the surface of mulberry leaves before feeding to silkworm. 3. For the investigation due to Perilla Ocymoides var application in stead of menthol plant ascribed in Paragraph (2) was obtained the same result. 4. As a conclusion of the study, the plantation of the both aromatical plants with mulberry trees is harmless for silkworm growing even though farmers worry about these to plant together with mulberry tree on mulberry farm.

• The Korean Journal of Physiology and Pharmacology
• /
• v.15 no.2
• /
• pp.115-122
• /
• 2011

The aim of this study was to investigate whether matrix metalloproteinase (MMP) inhibitors attenuate neuroinflammation in an ischemic brain following photothrombotic cortical ischemia in mice. Male C57BL/6 mice were anesthetized, and Rose Bengal was systemically administered. Permanent focal ischemia was induced in the medial frontal and somatosensory cortices by irradiating the skull with cold white light. MMP inhibitors, such as doxycycline, minocycline, and batimastat, significantly reduced the cerebral infarct size, and the expressions of monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and indoleamine 2,3-dioxygenase (IDO). However, they had no effect on the expressions of heme oxygenase-1 and neuroglobin in the ischemic cortex. These results suggest that MMP inhibitors attenuate ischemic brain injury by decreasing the expression levels of MCP-1, TNF-${\alpha}$, and IDO, thereby providing a therapeutic benefit against cerebral ischemia.