Effects of DCP on alcoholic fatty liver disease in rats via anti-inflammation and antioxidation / 中国药理学通报

Aim To study the effects of Dicliptera chinensis polysaccharide(DCP)on alcoholic fatty liver disease(AFLD)in rats based on anti-inflammation and antioxidation.Methods 60 rats were randomly divid-ed into six groups:control group,model group,silybin group and DCP of high,medium and low dose groups. The control group was fed with normal diet, other groups were fed with high sugar and high fat diet,and given 5% alcohol 5 mL·kg-1 by gavage.The alcohol consistency increased 5%every week until AFLD mod-els in rats were made after 7 weeks.Except control group,other groups were fed with high sugar and high fat diet,and given 35% alcohol 5 mL · kg-1 and DCP.All rats were killed after five weeks,and blood and liver tissues were collected.The activity of alanine aminotransaminase (ALT),aspartate aminotransferase (AST ), alkaline phosphatase (AKP ), triglyceride (TG),total cholesterol (TC ),low-density lipoprotein cholesterol(LDL-C)and high-density lipoprotein cho-lesterol(HDL-C)in serum were detected by using bio-chemical method. The contents of malondialdehyde (MDA),superoxide dismutase (SOD),reduced gluta-thione(GSH)in liver tissues were detected.The con-tents of tumor necrosis factor-α(TNF-α),interleukin-6 (IL-6 )and transforming growth factor-β1 (TGF-β1 ) were determined by enzyme-linked immunosorbent as-say(ELISA)in liver tissues.The liver tissues were ob-tained and histologic analysis was done through HE. Results DCP reduced the activity or content of ALT, AST,AKP,TG,TC,LDL-C,HDL-C,TNF-α,IL-6, TGF-β1 in serum and liver tissues of rats(P<0.05 ), and increased the activity or content of HDL-C,SOD and GSH (P<0.05 ).DCP could remarkably inhibit the NF-κB expression in liver tissues(P<0.01 ).The pathological examination indicated that DCP could ob-viously alleviate the inflammation and fat denaturation of the liver cells.Conclusion DCP can inhibit the de-velopment of AFLD.The mechanism may be related to antioxidation,free radical scavenging, inhibition of lipidperoxidation,anti-inflammation,and inhibition of the TGF-β1 and NF-κB expression.

Perioperative challenges in a patient of severe G6PD deficiency undergoing open heart surgery.

We describe a successful perioperative management of a case of 38-year-old male, presented with chronic jaundice with severe mitral stenosis and moderate tricuspid regurgitation; upon evaluation, he was found to have severe glucose-6-phosphate dehydrogenase (G6PD) deficiency. Usually, patients deficient in G6PD exhibit increased hemolysis andtherefore increased need for blood transfusion after cardiac surgery as well as impaired oxygenation in the postoperative period leading to prolonged ventilation. On reperfusion after a period of ischemia, the antioxidant system recruits all of its components in an attempt to neutralize the overwhelming oxidative stress of free radicals, as the free radical scavenging system is deficient in these patients, the chances of free-radical-induced injury is more. Our patient underwent mitral valve replacement and tricuspid annuloplasty under cardiopulmonary bypass with necessary precautions to reduce the formation of free radicals. Treatment was targeted toward theprevention of free radical injuryin the G6PD-deficient patient. He had an uneventful intraoperative and postoperative course.

Lithium Potentiates the FeCl2 Induced Free Radical Injury in Primary Mouse Cortical Cell Culture / 대한정신약물학회지

OBJECTIVES: For the past half century, lithium has been used for the acute and prophylactic treatment of bipolar disorder and recurrent depression. Recently, new pharmacological effects of Li+ have appeared, showing that Li+ can influence neuronal injury. We tested the effects of Li+ on free radical induced neuronal injury in primary murine cortical cell cultures. METHODS: Cortical cells were prepared from fetal mice (embryonic day 15) and exposed to 30 micrometer Fe2+ alone or with 5 mM Li+ or 5 mM Li+ alone for 24 hrs at Days in vitro (DIV) 14. Neuronal death was analyzed by measuring lactate dehydrogenase (LDH) release into media. The fluorescence of 2',7'-dichlorofluorescin (DCF) was measured in as a mean of estimating the formation of reactive oxygen species (ROS). RESULTS: Li+ alone does not produce neuronal injury itself but it potentiates Fe2+-induced neuronal injury through increasing the production of free radical. CONCLUSION: This study suggests that the effects of Li+ on neuronal survivorship may be injury type dependent and Li+ potentiate the free radical injury. Therefore in practice clinician should be cautious in using the lithium in the treatment of brain injured patients.

Study on the Mechanism of Kangnaoling Capsule Resisting Free Radical Injury of Vascular Dementia Rat / 中国中医药信息杂志

Objective To study the protection of Kangnaoling capsule to free radical injury and influence on the expression of caspase-3 and Bcl-2 in neuron of VD rat. Methods VD rat model was duplicated. Using spectrophotometry to detect contents of SOD, MDA and NO, spectro-fluorimeter to detect the expression of caspase-3, spectrophotometric method to detect the expression of Bcl-2 after traditional Chinese medicine interference. Results Kangnaoling capsule can markedly reduce the contents of MDA, raise contents of SOD and NO, degrade the expression of caspase-3, enhance the expression of Bcl-2. Conclusions Kangnaoling capsule can markedly protect VD rat from free radical injury, which probably correlated with increasing expression of Bcl-2, decreasing expression of caspase-3.

Mechanism of Hypoxia-Induced Cytotoxicity in Cultured Rat Retinal Neurons

Retinal neurons are highly vulnerable to hypoxia/ischemia. Excitotoxicity and free radical injury have been proposed as the major mechanisms of ischemic retinal injury have been proposed as the major mechanisms of ischemic retinal neuronal death. In the present study, we examined these possibilities in retinal cultures. Exposure of these cultures to hypoxia for 48 hr induced selective death of neurons. Addition of an antioxidiant trolox markedly attenuated hypoxiainduced retinal neuronal death, whereas addition of glutamate antagonists, MK-801 or CNQX,did not. Morphologically, hypoxic neuronal death in cultures was accompanied by cell body swelling, a feature of necrosis, yet simultaneously exhibited some features of apoptosis such as TUNEL positivity and protection by cycloheximide. However, unlike in classical programmed cell death, adding buthionine sulfoximine, a potent inhibitor of glutathione synthesis, completely reversed the protective effect of cycloheximide. The results have demonstrated that free radical injury is the main mechanism of neuronal death in the present retinal culture, and suggest an intriguing possibility that free redical injury may become a prominent mechanism, when excitotoxic injury is masked.

The effects of ascorbic acid on free radical injury in cultured retinal pigment epithelial cells

This study was conducted to investigate the effect of ascorbic acid on oxidative injury of cultured porcine retinal pigment epithelial (RPE) cells induced by t-butylhydroperoxide. The porcine RPE cells were cultured in Dulbecco's modified Eagle's medium and the culture medium was replaced with one containing 0.01 mM to 5 mM ascorbic acid and/or 0.2 mM t-butylhydroperoxide. After 2 hours incubation, the test medium was replaced with the control medium. The number of cells was counted with a Coulter counter after a 2-day incubation period. The medium was pretreated with 900 U/ml and the previous procedure was repeated to eliminate the toxic effects of hydrogen peroxide induced by ascorbic acid. Not only t-butylhydroperoxide (p 0.05). The cytotoxicity of t-butylhydroperoxide decreased when 1 mM and 5 mM of ascorbic acid was added to the culture media with catalase pretreatment (p = 0.0277). These results indicate that ascorbic acid was toxic to RPE cells in our culture model but this cytotoxicity was not detected in the presence of catalase. With catalase pretreatment, ascorbic acid in relatively high concentration provided protection against oxidative injury of t-butylhydroperoxide.

STUDY ON THE PROTECTIVE EFFECTS OF SELENIUM AND ZINC AGAINST OXIDATIVE DAMAGE INDUCED BY SOMAN IN RATS / 营养学报

Objective: To study the effect of free radical injury induced by Soman in rats and protection by Se/Zn. [WT5FZ]Methods: [WT5BZ]40 male rats were randomly divided into 4 groups, i.e., negative group, positive group, Se group and Zn group according to weights. The serum, cerebrum and liver VE content, nitrogen oxide synthase (NOS activity and T AOC (total antioxidative capacity) were determined. Results: The VE content and T AOC decreased markedly, and NOS activities increased significantly after Soman intoxication. The changes were less significant in Se/Zn supplemented group. Conclusion: The mechanism of free radical injury is indicated in Soman intoxication and Se/Zn supplementation has significant protection.