Saeng-Kankunbi-Tang () protects liver against oxidative damage through activation of ERK/Nrf2 pathway / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the cytoprotective effects of Saeng-kankunbi-tang (, SKT), a herbal prescription consisting of Artemisia capillaris and Alisma canaliculatum, and its underlying mechanism involved.</p><p><b>METHODS</b>In mice, blood biochemistry and histopathology were assessed in carbon tetrachloride (CCl4)-induced oxidative hepatic injury in vivo. The animal groups included vehicle-treated control, CCl4, SKT 500 mg/(kg day) CCl4+SKT 200 or 500 mg/(kg day). In HepG2 cell, tert-butyl hydroperoxide (tBHP) induced severe oxidative stress and mitochondrial dysfunction in vitro. The cyto-protective effects of SKT were determined by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay, flfluorescence activated cell sorting analysis and western blotting.</p><p><b>RESULTS</b>The administration of SKT prevented liver damage induced by CCl4 in mice, by inhibition of hepatocyte degeneration and inflflammatory cell infifiltration as well as plasma parameters such as alanine aminotransferase (P<0.01). Moreover, treatment with tBHP induced hepatocyte death and cellular reactive oxygen species production in hepatocyte cell line. However, SKT pretreatment (30-300 μg/mL) reduced this cell death and oxidative stress (P<0.01). More importantly, SKT inhibited the ability of tBHP to induce changes in mitochondrial membrane transition in cell stained with rhodamine 123 P<0.01). Furthermore, treatment with SKT induced extracellular signal-regulated kinases-mediated nuclear factor erythroid-2-related factor 2 (Nrf2) activation as well as the expressions of heme oxygenase 1 and glutamate- cystein ligase catalytic, Nrf2 target genes.</p><p><b>CONCLUSIONS</b>SKT has the ability to protect hepatocyte against oxidative stress and mitochondrial damage mediated by Nrf2 activation.</p>

Retrospective study on the bisphosphonate-related osteonecrosis of jaw

INTRODUCTION: The incidence of bisphosphonate-related osteonecrosis of the jaw (BRONJ) has increased gradually in patients who have undergone surgical treatment for osteomyelitis. In this study, a retrospective analysis of BRONJ patients was carried out using the data of osteomyelitis patients treated surgically. MATERIALS AND METHODS: Osteomyelitis patients, who underwent curettage, sequestrectomy, saucerization or decortications, and partial mandibulectomy at Seoul National University Dental Hospital from 2004 to 2010 were enrolled in this study. The patients were classified and categorized into two groups based on the surgical records and progress notes. One group comprised of patients with osteomyelitis and osteoporosis, and the other group included patients with osteomyelitis only. The epidemiological data of the BRONJ patients was analyzed to identify any trend in the incidence of BRONJ in osteomyelitis patients. RESULTS: Among 200 patients who underwent surgical intervention for osteomyelitis, 64 (32.0%) were identified as having osteoporosis as the underlying disease. In these 64 patients, more than 81.3% had been prescribed bisphosphonates. Females were far more affected by BRONJ than males. The incidence of BRONJ also increased with age. The posterior part of the mandible was affected more frequently by BRONJ. CONCLUSION: Although the availability of potent antibiotics and increased oral hygiene care can reduce the overall incidence of osteomyelitis, BRONJ can increase the total incidence. To prevent BRONJ, it is recommended that an oral examination be performed before prescribing bisphosphonates. Moreover, the patients should be educated about the potential risks of dental procedures that might be causal factors for BRONJ. Furthermore, patient swho take bisphosphonates for the treatment of osteoporosis should undergo periodic follow up oral examinations to prevent BRONJ.

Clinical analysis of early reoperation cases after orthognathic surgery

The factors influencing the relapse and recurrence of skeletal deformity after the orthognathic surgery include various factors such as condylar deviation, the amount of mandibular set-back, stretching force by the soft tissues and muscles around the facial skeleton. The purpose of this report is to recognize and analyze the possible factors of reoperation after orthognathic surgery, due to early relapses. Six patients underwent reoperation after the orthognathic surgeries out of 110 patients from 2006 to 2009 were included in this study. In most cases, clincal signs of the insufficient occlusal stability, anterior open bite, and unilateral shifting of the mandible were founded within 2 weeks postoperatively. Although elastic traction was initiated in every case, inadequate correction made reoperation for these cases inevitable. The chief complaints of five cases were the protruded mandible combined with some degree of asymmetric face and in the other one case, it was asymmetric face only. Various factors were considered as a major cause of post-operative instability such as condylar sagging, counter-clockwise rotation of the mandibular segment, soft tissue tension related with asymmetrical mandibular set-back, preoperatively existing temporomandibular disorder (TMD), poor fabrication of the final wafer, and dual bite tendency of the patients.

Evaluation of Apoptosis in the Normal Rat Brain after Intraoperative Irradiation

Radiation therapy is one of the most important treatment modalities following surgery of the primary malignant or metastatic brain tumors. But radiation can be harmful to normal healthy brain tissues around the tumor. There have been numerous reports of radiation induced damage such as delayed necrosis to human brain after therapeutic exposure. Apoptosis is a form of cell death with morphological and biochemical features that differ from those of necrosis. The aim of this study is to evaluate the apoptosis in normal rat brain after irradiation. Twenty one Sprague-Dawley rats were given a single dose of 10 Gy using high dose rate Ir-192 over 5 minutes at the right frontal region. Apoptosis was evaluated by the TUNEL method(In-situ end labelling technique) and mutant p53 protein, bc1-2 and bax genes were evaluated by immunohistochemical stain. Apoptosis was assessed at 1 week(group A, n=5), 2 week(group B, n=), 4 week(group C, n=), 6 week(group D, n=), 8 week(group E, n=) after irradiation. Apoptosis was noted with 20% of cases(1/5) in group A, 40% of cases(2/5) in group B, 60% of cases(3/5) in group C, 67% of cases(2/3) in group D and 100% of cases(3/3) in group E. Overall apoptosis positive rate was 52.4%(11/21). Apoptosis was most prominently found in external granular and external pyramidal layer(82%, 9/11) and found one case in internal pyramidal layer and the other one case in corticowhite matter junction. There were no positive stainning for mutant p53 protein, bc1-2 and bax gene in all cases pertaining to the phenomenon of apoptosis. In conclusion, apoptosis was evident in the rat brain after irradiation and the incidence of apoptosis was increased with time after irradiation. But the genes related to apoptosis after irradiation were not apparent in this study. Further evaluation including biochemical and clonogenic study needs to clarify the mechanism of apoptosis in normal brain after irradiation.

K-ras and p53 gene mutation in endometrial hyperplasia and adenocarcinoma / 대한산부인과학회잡지

Endometrial adenocarcinoma is the third common malignancy of female genital tract and categorized as estrogen-dependent tumor (type I) or not (type II). Type II endometrial adenocarcinoma more frequently occurs in oriental, which may arise from genetic alterations such as K-ras and p53. To identify whether the K-ras and p53 mutational activation are occurred during endometrial carcinogenesis, we examined point mutations of K-ras codon 12, 13, 61 (PCR-RFLP) and p53 exon 5, 6, 7, 8 (PCR-SSCP) in the 19 samples of endometrial adenocarcinoma. The 9 samples of normal endometrium and 24 samples of endometrial hyperplasia were also examined. K-ras codon 12 mutations were found in one of 3 cases of atypical hyperplasia (33.3%) and three of 19 cases of endometrial adenocarcinoma (15.7%). The correlation with K-ras mutation and endometrial hyperplasia/adenocarcinoma was statistically insignificant(p=0.306). p53 mutation was found in only one case of endometrial adenocarcinoma which concomitantly occurred with K-ras mutation. It could not be determined that K-ras mutation was early or late event during endometrial carcinogenesis due to a few cases of atypical hyperplasia and no K-ras mutation in the benign endometrial hyperplasia. The endometrial adenocarcinoma with K-ras mutation was observed in postmenopausal old age groups, and revealed moderate to severe histologic grade, early clinical stage, and negative lymph node metastasis.