To observe the effect of Shuangcao Tuihuang Granule-1 (SCTH-1) in treating severe jaundice of acute icterohepatitis and to study its mechanism. Methods: Thirty-four patients with severe jaundice of acute icterohepatitis were treated with conventional western medicine and SCTH-1, the therapeutic effects were analyzed and compared with that in the control group (treated with western medicine alone). In the animal experimental studies, the influences of SCTH-1 on acute liver injury, liver superoxide dismutase (SOD) and serum ALT and AST in mice were monitored. Results: The markedly effective rate in the treated group and the control group was 73.5% and 59.1% respectively, and the effective rate was 23.5% and 40.9% respectively. The markedly effective rate in the treated group was obviously higher than that in the control group (P＜0.05). Experimental study showed that SCTH-1 could reduce the level of serum transaminase and liver tissue damage in mice with acute liver damage. In addition, SCTH-1 could raise the activity of liver SOD (P＜0.05). Conclusion: SCTH-1 could accelerate the jaundice subsidence, improve the liver function and ameliorate the liver injury, its mechanism was possibly correlated with raising SOD activity and scavenging oxygen free radicals.

Effect of acupuncture on free radicals after spinal cord injury was observed in rats with experimental spinal cord injury (SCI). Results indicated that within 24 hours after SCI malondialdehyde (MDA) increased progressively, 2 hours after SCI it reached the peak; and the superoxide dismutase (SOD) activity decreased significantly at the same hours, the decrease being the most marked 2-6 hours after SCI. The MDA content in the acupuncture group was significantly lower (P<0.05) and the SOD activity higher (P<0.01) than that of the control group respectively. It is suggested that acupuncture inhibits production of MDA and increases the SOD activity.

AIM To study the role of lipid peroxides reaction on hepatic ischemia damage and the protective effects ofantioxidants (TMP, co-Q10).MgTHODS Twenty-four adult dogs were performed portacaval shunt and randomly put into 3 groups:group 1 (control group); 8 dogs with portacaval shunt (PCS group); group 2:8 dogs with portacaval shuntand only given antioxidants -TMP (ligustrazine) (PCS + TMP group); group 3:8 dogs with portacaval shuntand given antioxidants in combination with co-Q10, TMP and co-Q10 (PCS + TMP + co-Q10 group). Drugusage: TMP, 50 mg/ kg/ isolation day; coenzyme Q10, 1.5 mg/kg/isolation day; PCS + TMP, given up atthe end of 4 weeks after operation; and PCS + TMP + co-Q10, given up at the end of 8 weeks afteroperation. The experiment indices: super-peroxide dismutase (SOD), malondialdehyde (MDA), ALT,AST, AKP were all measured before operation, and 8 weeks after operation. The liver tissues were obtainedin the 4th week and 8th week respectively after operation and the changes of hepatic structures were observedunder light and electronic microscope.RESULTS There were obvious increase of MDA and decrease of SOD in PCS group, which was remarkablydifferent from pre-operation (P<0.01). In PCS + TMP group, there was no difference between pre-operation and within 4 weeks after operation (P>0.05). But it was remarkably different from PCS group(P<0.01). Beginning from the 5th week after operation, we stopped TMP (ligustrazine), as a result, theobvious increase of MDA, rapid decrease of SOD were found, but not different from PCS group (P >0.05).In PCS+ TMP+ co-QlO group, MDA increased slightlly, and SOD decreated, but it was superior to that inPCS and PCS + TMP groups. The data in PCS + TMP + co-Q10 group had statistical significance compared tothat in PCS+ TMP group (P<0.05) during 4 weeks after operation; but from the 5th to 8th week, there wasa remarkable difference (P<0.01). The results of ALT, AST and AKP showed remarkable differencebetween PCS + TMP + co-Q10, PCS group (P<0.01) and PCS + TMP compared to PCS + TMP + co-Q10(P<0.05). After stopping TMP, PCS + TMP were compared with PCS + TMP + co-Q10 (P<0.01). Thechanges in liver structures were fatty degeneration, atrophy and necrosis; decrease in rough surfacedendoplasmic reticulum (PER), mitochondrial swelling, partial mitochondria fusion, disappearance ofmitochondrial crista, diminution of Golgi body. The structures of liver cells in PCS + TMP and PCS + TMP +co-Q10 groups were superior to that in PCS group; but in the 8th week after operation, the liver structuralchanges bad no difference between PCS + TMP and PCS group. The results of light electronic microscopy inPCS + TMP + co-Q10 were better than that in PCS and PCS + TMP groups.CONCLUSION The over-activated lipid peroxides reaction may be one of the important factors of hepaticischemia damage after portacaval shunt; combined use of the antioxidants can enhance the protection fromthe hepatic ischemia damage.

AIM To study the relationship between the lipid peroxide (LPO) and superoxide dismutase (SOD) and thepathogenesis of gastrointestinal cancers.METHODS We investigated the SOD activity and LPO levels in blood and mucosa of patients withesophageal (EC), gastric (GC) and colorectal cancer (CC), gastric ulcer (GU) and compared with normalesophagus (NE), stomach (NS) and colon (NC). respectively, 287 patients who underwent endoscopy werestudied. SOD activity of the tissue and blood was determined using SUN's adrenaline auto oxidation method.LPO levels were determined according to YU's method.RESULTS The SOD activity and LPO level in blood and mucosa are shown in the Table 1 (x±Sx).Table 1 SOD and LPO in blood and tissues of patients with gastrointestinal cancers SOD(U／mg protein) LPO(U／mg)Groups n Tissue blood Tissue BloodNormal stomachGastric ulcerGastric cancerNormal esophagusEsophageal cancerNormal colonColon cancer 60 42 43 32 52 28 30 1.90±0.18 0.64±0.40a 0.37±0.24a 1.17±0.70 0.39±0.30a 0.81±0.36 0.31±0.17b 33.70±1.73 25.50±0.67b 27.86±1.02b 30.80±3.78 28.23±10.63 20.97±4.77 19.35±7.32 0.01±0.004 0.05±0.010b 0.06±0.021b 0.014±0.005 0.061±0.033b 0.012±0.003 0.069±0.015b 0.83±0.01 0.11±0.02 0.12±0.03 0.08±0.02 0.11±0.02 0.08±0.03 0.11±0.02aP<0.001, bp<0.01 vs corresponding normal controls, respectively.CONCLUSION SOD activity of the tissue is significantly decreased in EC. GC and CC. LPO levels weresignificantly higher than those of corresponding normal tissue. These results suggest that mucosal SOD andLPO levels are closely related to the pathogenesis of the gastrointestinal cancers.

In addition to its lipid-lowering effect, atorvastatin exerts anti-inflammatory and antioxidant effects as well. In this study, we hypothesized that atorvastatin could protect against cerebral isch-emia/reperfusion injury. The middle cerebral artery ischemia/reperfusion model was established, and atorvastatin, 6.5 mg/kg, was administered by gavage. We found that, after cerebral ischemia/reperfusion injury, levels of the inflammation-related factors E-selectin and myeloperoxidase were upregulated, the oxidative stress-related marker malondialdehyde was increased, and super-oxide dismutase activity was decreased in the ischemic cerebral cortex. Atorvastatin pretreatment signiifcantly inhibited these changes. Our ifndings indicate that atorvastatin protects against ce-rebral ischemia/reperfusion injury through anti-inlfammatory and antioxidant effects.

Ganoderma lucidum is a traditional Chinese medicine, which has been shown to have both an-ti-oxidative and anti-inlfammatory effects, and noticeably decreases both the infarct area and neuronal apoptosis of the ischemic cortex. This study aimed to investigate the protective effects and mechanisms of pretreatment with ganoderma lucidum (by intragastric administration) in cerebral ischemia/reperfusion injury in rats. Our results showed that pretreatment with ganoder-ma lucidum for 3 and 7 days reduced neuronal loss in the hippocampus, diminished the content of malondialdehyde in the hippocampus and serum, decreased the levels of tumor necrosis fac-tor-αand interleukin-8 in the hippocampus, and increased the activity of superoxide dismutase in the hippocampus and serum. hTese results suggest that pretreatment with ganoderma lucidum was protective against cerebral ischemia/reperfusion injury through its anti-oxidative and an-ti-inlfammatory actions.

Edaravone has been shown to reduce ischemia/reperfusion-induced peripheral nerve injury. However, the therapeutic effect of edaravone on peripheral nerve injury caused by mechanical factors is unknown. In the present study, we established a peripheral nerve injury model by crushing the sciatic nerve using hemostatic forceps, and then administered edaravone 3 mg/kg intraperitoneally. The sciatic functional index and superoxide dismutase activity of the sciatic nerve were increased, and the malondialdehyde level was decreased in animals in the edaravone group compared with those in the model group. Bcl-2 expression was increased, but Bax expres-sion was decreased in anterior horn cells of the L4-6 spinal cord segments. These results indicated that edaravone has a neuroprotective effect following peripheral nerve injury caused by mechan-ical factors through alleviating free radical damage to cells and inhibiting lipid peroxidation, as well as regulating apoptosis-related protein expression.

Green tea polyphenols are strong antioxidants and can reduce free radical damage. To investigate their neuroprotective potential, we induced oxidative damage in spinal cord neurons using hy-drogen peroxide, and applied different concentrations (50-200 μg/mL) of green tea polyphenol to the cell medium for 24 hours. Measurements of superoxide dismutase activity, malondial-dehyde content, and expression of apoptosis-related genes and proteins revealed that green tea polyphenol effectively alleviated oxidative stress. Our results indicate that green tea polyphenols play a protective role in spinal cord neurons under oxidative stress.

Zinc supplementation can help maintain learning and memory function in rodents. In this study, we hypothesized that zinc supplementation could antagonize the neurotoxicity induced by aluminum in rats. Animals were fed a diet containing different doses of zinc (50, 100, 200 mg/kg) for 9 weeks, and oral y administered aluminum chloride (300 mg/kg daily) from the third week for 7 consecutive weeks. Open-field behavioral test results showed that the number of rearings in the group given the 100 mg/kg zinc supplement was significantly increased compared with the group given the 50 mg/kg zinc supplement. Malondialdehyde content in the cerebrum was significantly decreased, while dopamine and 5-hydroxytryptamine levels were increased in the groups given the diet plemented with 100 and 200 mg/kg zinc, compared with the group given the diet supplemented with 50 mg/kg zinc. The acetylcholinesterase activity in the cerebrum was significantly decreased in the group given the 100 mg/kg zinc supplement. Hematoxylin-eosin staining revealed evident patho-logical damage in the hippocampus of rats in the group given the diet supplemented with 50 mg/kg zinc, but the damage was attenuated in the groups given the diet supplemented with 100 and 200 mg/kg zinc. Our findings suggest that zinc is a potential neuroprotective agent against alumi-num-induced neurotoxicity in rats, and the optimal dosages are 100 and 200 mg/kg.

家族性肌萎缩侧索硬化症的病因研究进展

肌萎缩侧索硬化症(amyotrophic lateral sclerosis,ALS)是选择性侵犯上、下运动神经元的慢性进行性变性疾病,可分为散发性ALS和家族性ALS(FALS).FALS约占10%,表现为常染色体显性遗传或常染色体隐性遗传.FALS病因尚未完全明确.随着分子遗传学的研究发展,目前,FALS分为5种类型[1,2]:ALS1、ALS2、ALS3、ALS4、ALS5.ALS1为常染色体显性遗传,基因定位于21q22.1,是由于铜锌超氧化物岐化酶(CuZn superoxide dismutase,SOD1)基因突变所致.青年型ALS是指在儿童或青少年期起病的FALS.表现为常染色体隐性遗传的青年型ALS可分为ALS2和ALS5.前者基因定位于2q33,后者基因定位于15q15.1～q21.1.表现为常染色体显性遗传的青年型ALS,病程进展缓慢,基因定位于9q34,称之为ALS4.而成人起病,呈常染色体显性遗传的FALS,基因定位既不在21号染色体上,又与SOD1基因突变无关,可能位于其他基因位点,被命名为ALS3.

网状减张缝合提高张力皮瓣存活率的实验研究

Objective To observe effects of meshed relaxing short incisions on the level of superoxide dismutase and malondialdehyde in rat tension skin flap, and to investigate the mechanism of meshed relaxing short incisions (MRSI) on wound healing process of tension skin flap. Method An experimental model was designed to investingate the changes of superoxide dismutase (SOD) and malondialdehyde (MDA) in rat skin flap tissue each period of wound healing (12h, 24h, 48h, 72h after suture). In the meantime, the biochemical reaction were employed. Results Our results showed that SOD content in rat skin flap tissue from MRSI group were significant higher than that of hypertension group (P≤ 0.05), while MDA content was significantly lower (P≤ 0.05). Conclusion The decrease of MDA contents may be one of the causes that MRSI improves microcirculation of skin flap, and reduces edema and facilitates healing of skin flap.

早期肠道营养对烧伤大鼠模型内脏缺血损害的效应

AIM:To compare the effects of early enteral nutrition and early parenteral nutrition on ameliorating visceral ischemia and relieving free radical damage.METHODS:66 Wistar rats were divided into 3 groups: control group(C),parenteral nutrition group( PN) and enteral nutrition group( EN), PN and EN groups made up of 30% TBSAⅢ degree burn model.We delivered nutrient solution with same calorie and calorie- nitrogen ratio via vein or enteral tract respectively.Blood flow of liver,kidney and change of SOD of heart,liver and kidney at 6,12,24,48,72 h after burn were tested.RESULTS:Tissue blood flow and SOD of EN group were higher than those of PN group in many phase( P< 0.05-0.01) .CONCLUSION: Early enternal nutrition can relieve the increase of visceral vascular permeability and damage of oxygen free radical.

呆聪液对老年痴呆大鼠血清酶及LPO的影响

Objective To explore the effect of Daicong solution (DCS) on aged rats dementia model.Method The experiment used 22 month old rats whose basal nuclei was destroyed by bilateral electrolytic method as model for aged rats dementia.They were treated with DCS for a month.Then the level of superoxide dismutase (SOD),lipid peroxide(LPO),monoamine oxidase (MAO) and cholinesterase(CHE) in the serum was measured. Result Compared with the control,the activity of SOD increased markedly(P< 0.01), the content of LOP and activity MAO and CHE were decreased(P< 0.01).Conclusion DCS is effective in treating the aged dementia.

旅途精神病患者血清超氧化物歧化酶活性及丙二醛水平

背景 氧化应激是一种神经毒性因素,可能会促使急性精神病的发生.目的 评估旅途精神病(travel-induced psychosis)与氧化应激的关系.方法 对乘坐长途火车诱发的 21 例旅途精神病住院患者,在其入院时采用简明精神病评定量表(Brief Psychiatric Rating Scale,BPRS)评定精神症状,入院次日清晨测定其血清超氧化物歧化酶(super oxide dlsmutase,SOD)活性和丙二醛(malondialdehyde,MDA)含量;待患者精神病性症状缓解后(通常为小剂量抗精神病药治疗后 2~6天),再次进行上述检测.选取性别、年龄匹配的 21 名健康志愿者为对照组,比较患者与对照者的血清SOD活性和MDA含量.结果 入院时患者的血清SOD活性和MDA含量均高于对照组.精神症状缓解后,患者的BPRS评分、血清SOD活性和MDA含量均显著下降,但后两者仍高于对照组.入院时患者的BPRS总分与SOD活性呈正相关(r=0.32,p=0.164),与MDA含量也呈正相关(r=0.34,p=0.126),但均无统计学意义.治疗后BPRS总分的下降与SOD活性的下降弱相关(r=0.28,p=0.217),也与MDA含量的下降也呈弱相关(r=0.29,p=0.211).结论 研究结果提示,氧化应激的神经毒性作用与旅途精神病的发生直接相关.这或许能够帮助我们理解其他急性精神病性障碍(如精神分裂症)的发生.

特发性膜性肾病发病机制的研究现状

特发性膜性肾病(idiopathic membranous nephropathy,IMN)系针对肾小球脏层上皮细胞膜抗原成分、由自身抗体介导、补体参与的器官特异性自身免疫病[1].近年人们对膜性肾病(membranous nephropathy,MN)的发病机制的研究取得了实质性进展[2].这些研究包括靶抗原如中性肽链内切酶(neutral peptide chain enzymes,NPE)[3]、抗M型磷脂酶A2受体(M-type phospholipase A2 receptor,PLA2R)[4]、醛糖还原酶(aldose reductase,AR)和超氧化物歧化酶(manganese superoxide dismutase,SOD2)[5]的认识,体液免疫介导的膜攻击复合物C5b-9致足细胞的损伤,其发病原因仍未明.本文就其研究现状介绍如下.

AIM: To study the protecitve mechanism of Ligustrazine (LT), Shenmai Parenteral Injection (SPI), combination of Ligustrazine and Shenmai Parenteral Injection (LSP) to myocardial injury after brain ischemia-reperfusion in aged rats from the change in ATPase and free radical in order to provide theoretical basic for prevention and cure of cerebral infarction. METHODS: Aged rats (more than 20 months) were divided into model group, control group, Nimotop group, LT group, SPI group and LSP group. We measured the following items in aged rats with 60 min of reperfusion after 30 min of brain ischemia: the content of MDA, the activities of superoxide dismutase (SOD), lactic dehydrrogenase (LDH), creatine phosphokinase (CPK), ATPase. RESUTLS: The CPK and LDH activities in the model rats increased obviously. The serum CPK activity in the LSP group, the LT group, nimotop group was lower than those in the model group obviously. The serum LDH activities in LT group and SPI group were obviously lower compared with those in the model group. The activity of Na＋-K＋-ATPase and Ca2＋-ATPase in model group was decreased. Contrast to the model group, the activity of Na＋-K＋-ATPase in LSP group, Nimotop group, LT group and the activities of Ca2＋-ATPase in the LSP group were higher. The serum MDA/SOD ratio was larger than that in the control group. The decrease in myocardial SOD activity and the increase in the MDA level, MDA/SOD ratio in the model group showed significant difference compared with that in the control. The MDA level in the LSP group was lower than that in the model group. The increase in myocardial SOD activity and decrease in MDA, MDA/SOD ratio were obvious in the LSP group compared with the model group. CONCLUSION: The myocardial injury after brain ischemia-reperfusion in aged rats was related to the decrease in the activity of Na＋-K+-ATPase and injury of free radical. LT, SPI, LSP and Nimotop could prevent this inury. Nimotop and LT could enhanced the activity of Na+-K+-ATPase obviously. SPI could enhance the activity of Ca2＋-ATPase and restrain the injury of free redical and lipid peroxidation. This may be the mechanism of restraining myocardial injury after brain ischemia-reperfusion.

氧自由基与超氧化物歧化酶的文献综合利用(三)

近年来,国外对氧自由基(OFR)和超氧化物歧化酶(SOD)的研究,尤其是在神经系统方面,已有突破性的进展,从量变的研究跃升到质变的研究.有研究表明,不仅SOD的量变影响疾病的发生发展过程,而且SOD的质变(突变)也会导致疾病的发生[1-3].甚至有研究表明,在一些细胞中发现了OFR与NO一样,对鸟苷酸环化酶和其他信号系统有调节作用[4].