口服维生素D在妊娠期细菌性阴道病治疗中的疗效研究

目的 探讨维生素D口服联合维生素C、乳酸杆菌制剂阴道用药在治疗妊娠期细菌性阴道病中的疗效。方法 100例妊娠期的细菌性阴道病患者,随机分为对照组和观察组,各50例。对照组采用维生素C、乳酸杆菌制剂阴道用药方法治疗;观察组采用维生素D口服联合维生素C、乳酸杆菌制剂阴道用药方法治疗。比较两组的临床疗效。结果 经过1周的治疗后,对照组有41例患者治疗有效,观察组有48例治疗有效;停药1周后,对照组复发7例,观察组有1例复发。两组疗效比较差异具有统计学意义(P<0.05)。结论 采用维生素D口服联合维生素C、乳酸杆菌制剂阴道用药的方法 ,在治疗妊娠期细菌性阴道病的应用中,治疗效果好,减少了复发率,减轻了患者的经济负担,值得在妇科疾病治疗中广泛的推广应用。     

丹参治疗急性重型颅脑损伤的临床应用

为观察丹参治疗急性重型颅脑损伤的临床效果,按标准选取急性重型颅脑损伤30例,随机分成对照组和观察组各15例。对照组行常规治疗,观察组在常规治疗的基础上加用丹参治疗。治疗前和治疗后24h、48h、72h、1周及2周分别采取肱静脉血测血浆内皮素（ET）含量,检测观察组病人的血压。两组病人分别于治疗前和治疗后3天、1周分别行Glasgow昏迷评分（GCS）。治疗后72h、1周行腰椎穿刺术,检测颅内压力,比较两组的疗效。结果表明,治疗后观察组血浆ET含量和颅内压力明显低于对照组,GCS高于对照组,差异均有统计学意义（P〈0.05）;观察组丹参治疗前后血压变化不明显,差异无统计学意义（P〉0.05）。结论：丹参对急性重型颅脑损伤病人具有明显的临床治疗效果。     

急性非ST段抬高性心肌梗死治疗药物的选择

目的 观察替罗非班治疗急性非ST段抬高性心肌梗死的临床疗效.方法 将110例患者随机分为2组,每组55例.两组患者入院后均给予常规治疗,观察组同时给予替罗非班治疗.两组均于用药后4h、24h、72h观察ST段恢复情况.结果 治愈率观察组为80.00%,对照组为67.27%;总有效率观察组为92.73%,对照组为85.45%.两组比较差异有统计学意义(P＜0.05).两组治疗后4h、24h、72h ST段恢复情况比较差异有统计学意义(P＜0.05).结论 在常规治疗的基础上使用替罗非班治疗急性非ST段抬高性心肌梗死临床疗效显著,可使病变的ST段恢复正常.     

环磷腺苷葡胺联合维生素C治疗儿童心肌损伤的疗效及对肌酸激酶和肌酸激酶同工酶水平的影响

目的 探讨环磷腺苷葡胺联合维生素C治疗儿童心肌损伤的临床疗效。方法 选取2019年1月至2022年3月期间滕州市中心人民医院收治的70例心肌损伤患儿,按数字随机表法分为两组,即对照组35例,采用维生素C治疗;观察组35例,在对照组用药基础上采用环磷腺苷葡胺治疗;对比两组临床效果、心肌酶谱、肌酐蛋白I(cTnI)、心电图改善情况。结果 观察组治疗48 h的临床效果91.43%高于对照组的68.57%,临床症状、心肌酶谱、心电图恢复正常时间均短于对照组(P<0.05)。观察组治疗后CK、CK-MB、cTnI水平低于对照组,左室等容收缩、舒张时间(ICT、IRT)、左心室Tei指数低于对照组,左室射血分数(LVEF)高于对照组(P<0.05)。观察组治疗后超氧化物歧化酶(SOD)、白介素(IL)-6、IL-8及肿瘤坏死因子(TNF-α)低于对照组(P<0.05)。两组不良反应比较差异无统计学意义(P>0.05)。结论 环磷腺苷葡胺联合维生素C可提高儿童心肌损伤治疗效果,促进心电图恢复,修复心肌损害。     

雌孕激素联合应用和达英-35治疗青春期功血临床疗效观察

目的：探讨雌孕激素联合应用和炔雌醇环丙孕酮片(达英-35)治疗青春期功血的临床疗效及安全性。方法60例青春期功血患者，随机分为对照组与观察组，各30例，对照组患者采用雌孕激素联合应用治疗，观察组患者采用达英-35治疗，观察两组患者的止血效果、再次出血以及用药后不良反应等情况。结果观察组患者用药后48 h以及72 h内的完全止血率优于对照组患者(P<0.05)，观察组患者治疗总有效率为100.0%，对照组患者90.0%，组间相比差异具有统计学意义(P<0.05)。结论达英-35在治疗青春期功血患者方面疗效优于雌孕激素联合应用，用药不良反应较少，值得大力推广应用。     

静脉推注呋塞米配合治疗输尿管结石的观察与护理体会

目的观察静脉推注呋塞米与静脉滴注呋塞米在配合治疗输尿管结石临床疗效差异及护理体会。方法在同等计量下观察组采用静脉滴注呋塞米,辅以解痉药物,对照组采用静脉推注呋塞米辅以解痉药物,观察用药后1h、3h、24h、24h以上患者疼痛缓解情况及结石的排出情况。结果观察组24h总有效率77.5%,对照组总有效率45%,观察组疗效优于对照组。结论静脉推注呋塞米联合解痉药物治疗输尿管结石疗效迅速、费用低、患者痛苦少,值得在临床推广应用。现将临床观察与护理体会汇报如下。     

纳洛酮、氨茶碱对早产儿原发性呼吸暂停的疗效比较

目的：评估纳洛酮与氨茶碱两组方案治疗早产儿原发性呼吸暂停的疗效差异。方法：42例患儿随机分成纳洛酮治疗组20例、氨茶碱治疗组22例。结果：用药1h、1～24h、24～72h，两组治疗效果在统计学上有显著差异，72h后无统计差异。结论：用药72h内纳洛酮效果优于氨茶碱。     

泮托拉唑治疗急性酒精中毒后胃黏膜损伤的疗效观察

目的:观察泮托拉唑治疗急性酒精中毒后胃黏膜损伤的临床疗效。方法:将急性酒精中毒后急性胃黏膜损伤患者60例随机均分为治疗组和对照组。治疗组30例采用泮托拉唑40 mg.d-1,q12h,静脉滴注;对照组30例采用西咪替丁0.6 g,bid,静脉滴注。观察2组患者用药72 h内临床症状的缓解情况。结果:治疗组显效率为66.7%,总有效率为96.7%;对照组显效率为26.7%,总有效率为76.7%,2组比较差异有统计学意义(P<0.05)。结论:泮托拉唑治疗急性酒精中毒后胃黏膜损伤的疗效显著。     

还原型谷胱甘肽对严重烧伤延迟复苏肝脏保护作用的临床观察

目的观察还原型谷胱甘肽对治疗严重烧伤延迟复苏患者肝功能异常的临床结果。方法选择严重烧伤后6h内未进行液体复苏、肝功能异常患者30例,随机分为两组,治疗组静脉滴注还原型谷胱甘肽,对照组静脉滴注维生素C,分别于用药前、用药后24h,用药后48h采取静脉血检测肝功能指标。结果治疗前后肝功能指标治疗组变化明显（P〈0.05）。结论还原型谷胱甘肽对烧伤所致肝功能异常的降酚作用迅速,近期疗效显著,应用安全。     

大剂量维生素C联合纳洛酮治疗新生儿缺氧缺血性脑病疗效观察

目的观察大剂量维生素C和纳洛酮治疗新生儿缺氧缺血性脑病的疗效。方法对90例患儿随机分为2组,治疗组在对照组治疗基础上,加用大剂量维生素C每次250～300mg.kg-1,观察两组的治疗和随访结果。结果两组治疗方法根据用药时间、症状恢复情况及观察结果比较,治疗组与对照组有明显差异。结论大剂量维生素C联合纳洛酮治疗新生儿缺氧缺血性脑病疗效显著。     

天麻糖复合物对大鼠缺血/再灌注模型视网膜的影响

目的观察天麻糖复合物(polysaccharides from Gastro-d ia elata B lum e,GEP)对大鼠视网膜缺血/再灌注(retinal is-chem ia reperfusion,R IR)后视网膜超氧化物歧化酶(superox-ide d ismutase,SOD)、丙二醛(m alond ialdehyde,MDA)、一氧化氮(n itric oxide,NO)含量及视网膜形态的影响。方法采用前房灌注液体形成16 kPa高眼压而建立R IR模型。SD大鼠随机分为:GEP小剂量组、中剂量组、大剂量组、维生素E组、阴性对照组,缺血60 m in后恢复血流,分别于再灌注60 m in,24 h和72 h检测视网膜组织中MDA(比色法),SOD(比色法)、NO(硝酸还原酶法)含量及视网膜光学显微镜的组织学观察。结果GEP干预后,再灌注60 m in,24 h和72h后中、大剂量干预组视网膜中MDA含量均明显低于阴性对照组(P<0.05);SOD含量均明显高于阴性对照组(P<0.05);NO含量在再灌注24~72 h时间段内明显低于阴性对照组(P<0.05),GEP干预组视网膜组织形态学损害较阴性对照组明显减轻。结论GEP对缺血/再灌注的视网膜具有保护作用。     

The effects of organophosphate insecticide methidathion on lipid peroxidation and anti-oxidant enzymes in rat erythrocytes: role of vitamins E and C

The effects of organophosphate insecticide methidathion (MD) on lipid peroxidation and anti-oxidant enzymes and the ameliorating effects of a combination of vitamins E and C against MD toxicity were evaluated in rat erythrocytes. Experimental groups were: control group, MD-treated group (MD), and MD + vitamin E + vitamin C-treated group (MD + Vit). MD and MD + Vit groups were treated orally with a single dose of 8 mg/kg MD body weight at 0 hour. Vitamins E and C were injected at doses of 150 mg/kg body weight, i.m. and 200 mg/kg body weight, i.p., respectively, 30 min after the treatment of MD in the MD + Vit group. Blood samples were taken 24 hours after the MD administration. The level of malondialdehyde (MDA), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were studied in the erythrocytes. MDA level increased significantly in the MD group compared to the control group (P < 0.05) and decreased significantly in the MD + Vit group compared to the MD group (P < 0.05). The activities of SOD, GSH-Px, and CAT decreased in the MD group compared to the control group (P < 0.05). Only GSH-Px activity increased in the MD + Vit group compared with the MD group. These results suggest that treating rats with MD increases LPO and decreases anti-oxidant enzyme activities in erythrocytes. Furthermore, single-dose treatment with a combination of vitamins E and C 30 min after the administration of MD can reduce LPO caused by MD.     

牛磺酸对大鼠视网膜缺血再灌注损伤的影响

目的观察牛磺酸对大鼠视网膜缺血再灌注损伤（retinal ischemia-reperfusion，RIR）的影响及其作用机制。方法将120只大鼠随机分为3组：对照组、缺血组、保护组，采用前房灌注液体形成14．63kPa高眼压1h的方法，建立RIR模型，连续3d，2次／d，腹腔注射10％的牛磺酸，剂量为100mg／kg，于手术前30min加注1次。对照组给予同等剂量的生理盐水。两组缺血60min后，分别再灌注0、2、6、12、24、48、72h用比色法进行视网膜SOD、MDA、NO的测定；用光镜测量包埋切片的平均视网膜内层厚度（meanthicknessofinnerretinallayer，MTIRL）。结果牛磺酸能显著对抗大鼠视网膜缺血再灌注后MDA和NO水平的升高，同时能改善平均视网膜内层厚度的变化，但对SOD的作用不确定。结论牛磺酸可减轻大鼠视网膜缺血再灌注后的损伤。     

The effects of desferrioxamine on cisplatin-induced lipid peroxidation and the activities of antioxidant enzymes in rat kidneys

Cisplatin-induced nephrotoxicity is associated with an increase in lipid peroxidation and oxygen free radicals in rat kidneys. In this study, the effects of desferrioxamine were compared to vitamin C and E on cisplatin-induced lipid peroxidation and antioxidant enzyme activities in rat kidneys. Rats were divided into five groups, with 15 Wistar rats in each group. In the control group, rats received 1 mL/100 g isotonic saline solution intraperitoneally (i.p.). In Group II, 10 mg/kg cisplatin i.p. was injected to rats. Thirty minutes before the same dosage of cisplatin administration, 100 mg/kg i.p. vitamin C or E was given to rats in groups III and IV, respectively. Rats in Group V received 250 mg/kg desferrioxamine i.p., before the same dose of cisplatin administration. All rats were killed by cervical dislocation after 72 hours. The kidneys were immediately removed and washed in cold saline. Spectrophotometric method was used for all analyses. While catalase, glutathione reductase (GR), and superoxide dismutase (SOD) levels were found to be significantly decreased (P < 0.001), malondialdehyde (MDA) (P < 0.05) and hydrogen peroxide (H2O2) (P < 0.001) levels were significantly increased in the cisplatin group when compared to the controls. MDA levels were decreased by desferrioxamine (P < 0.005) as well as vitamin C and E (P < 0.05 and P < 0.001, respectively). These three compounds induced a significant increase in SOD levels (P < 0.05), but only in the vitamin C group, were SOD levels not significantly different than the levels of the controls (P > 0.05). In the desferrioxamine (P < 0.05), vitamin C and E groups (P < 0.001 for both), the cisplatin elevated H2O2 levels were decreased. None of these drugs had any effect on GR and catalase levels (P > 0.05). Desferrioxamine is useful to prevent cisplatin-induced lipid peroxidation, however, vitamin C and E are more effective on antioxidant enzymes than desferrioxamine.     

Cytotoxicity in ciprofloxacin-treated human fibroblast cells and protection by vitamin E

Quinolones (Qs) were shown to have cytotoxic effects in various cell lines including human carcinoma cells; however, mechanism of these effects was not fully understood. To investigate the possibility of the involvement of an oxidative stress induction in this mechanism of action, we examined viability of human fibroblast cells exposed to a Q antibiotic, ciprofloxacin (CPFX), and measured lipid peroxidation and total glutathione (GSH) levels, and activities of catalase (Cat), superoxide dismutases (SODs), glutathione peroxidase (GPx). The effects of vitamin E pretreatment on those parameters were also examined. Our results showed that the effect of CPFX on the viability of the cells, as determined by neutral red uptake assay, was time dependent. Cytotoxicity was not observed in the concentration range of 0.0129-0.387 mM CPFX when the cells were incubated for 24 hours. However, significant level of cytotoxicity was observed at concentrations 0.129 and 0.194 mM, and >0.129 mM, following 48 and 72 hours of exposure, respectively. When the cells were exposed to 0.194 mM CPFX for 48 hours, the level of lipid peroxidation increased and the content of total GSH decreased significantly; activities of total SOD, Mn SOD and CuZn SOD did not change; the decrease observed in the activity of Cat was not significant; and the activity of GPx was highly variable. Vitamin E pretreatment of the cells provided significant protection against CPFX-induced cytotoxicity; lowered the level of lipid peroxidation significantly, but increased the total GSH content only moderately; no change was observed in the activities of Cat and total SOD, but a significant increase in Mn SOD and a significant decrease in CuZn SOD were noticed. These results suggested that CPFX-induced cytotoxicity on human fibroblast cell cultures is related to oxidative stress, and vitamin E pretreatment can afford a protection.     

依达拉奉在急性脑梗死时抗氧化及神经内皮保护作用的研究

目的研究依达拉奉对急性脑梗死患者血清超氧化物歧化酶（SOD）、丙二醛（MDA）表达的影响。并分析其临床意义。方法选择急性脑梗死患者120例随机分为对照组（常规治疗）和依达拉奉组（依达拉奉＋常规治疗,依达拉奉30mg＋0．9％氯化钠溶液100ml,静脉滴注,2次／d,连续14d）,每组60例,检测治疗前、发病72h和治疗后7、14d患者血清中SOD、MDA的变化。结果依达拉奉组治疗后血清SOD升高、MDA减少,发病72h和治疗后7d与对照组比较差异有统计学意义（P〈0．05）。结论急性脑梗死患者应用依达拉奉治疗可以降低氧自由基水平,减轻对缺血脑细胞的损害。     

In vivo changes in antioxidant systems and protective role of melatonin and a combination of vitamin C and vitamin E on oxidative damage in erythrocytes induced by chlorpyrifos-ethyl in rats

Reactive oxygen species (ROS) may be involved in the toxicity of chlorpyrifos-ethyl (CE) [O,O-diethyl-O-(3,5,6-trichloro-2-pyridyl)phosphorothioate]. We have, therefore, examined the in vivo effects of CE on the rat erythrocyte antioxidant system and evaluated the ameliorating effects of melatonin and a combination of vitamin E and vitamin C on the oxidative damage induced by CE. The experimental groups were: (1) control group, (2) CE-treated group (CE), (3) vitamin E plus vitamin C treatment group (Vit), (4) melatonin-treated group (Mel), (5) vitamin E plus vitamin C plus CE treatment group (Vit + CE), and (6) melatonin plus CE treatment group (Mel + CE). Vitamin E and vitamin C were administered intramuscularly once a day for 6 consecutive days at 150 and 200 mg/kg, respectively, in the Vit and Vit + CE groups. Melatonin was administered intramuscularly at 10 mg/kg per day for 6 consecutive days in the Mel and Mel + CE groups. At the end of the fifth day, the rats of CE, Vit + CE and Mel + CE groups were treated orally with the first of two equal doses of 41 mg/kg CE, the second oral dose being given 21 h later. Blood samples were taken 24 h after the first CE administration. Levels of thiobarbituric acid reactive substance (TBARS), antioxidant defence potential (AOP), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were determined in erythrocytes. In comparison with the control group, oral administration of CE significantly (P < 0.05) stimulated TBARS activity while significantly (P < 0.05) inhibiting AOP and the activities of SOD and CAT. However, GSH-Px activity remained unchanged by CE treatment. Treatment with melatonin and vitamins E plus C significantly (P < 0.05) reduced the CE-induced increase of TBARS, and overcame the inhibitory effect of CE on SOD and CAT, but not on AOP. Melatonin treatment significantly (P < 0.05) increased only GSH-Px activity, irrespective of the effect of CE. These results suggest that CE treatment increases in vivo lipid peroxidation and decreases antioxidant defence by increasing oxidative stress in erythrocytes of rats, and melatonin and a combination of vitamin E and vitamin C can reduce this lipoperoxidative effect.     

Protective effect of L-carnitine and coenzyme Q10 on CCl₄-induced liver injury in rats

This study provides an information about the mechanisms of liver injury induced by CCl(4), and determines the influence of administration of L-carnitine or/and CoQ10 as prophylactic agents against CCl(4) deteriorative effect. The study was carried out on 80 adult male albino rats divided into eight groups, 10 animals each, as follows: four normal groups (control, treated with L-carnitine, treated with CoQ10, and treated with a combination of Lcarnitine and CoQ10) and four liver injury groups treated with CCl(4) (control, treated with L-carnitine, treated with CoQ10, and treated with a combination of L-carnitine and CoQ10). Liver injury was induced by s.c. injection of a single dose of CCl(4) (1 ml/kg). L-carnitine (50 mg/kg/day) was given i.p. for four successive days 24 hours before CCl(4) injection, and CoQ10 (200 mg/kg) was given as a single i.p. dose 24 hours before CCl(4) injection. Animals were sacrificed 24 hours after CCl(4) injection, blood samples were withdrawn and liver tissue samples were homogenized. The levels of the following parameters were determined: hepatic reduced glutathione, serum ALT and AST, hepatic lipid peroxides, hepatic vitamin C, hepatic and serum total protein, serum albumin, serum sialic acid, serum nitrite, and serum and hepatic total LDH activities and LDH isoenzymes. The obtained data revealed that CCl(4) injection produced a significant decrease in reduced glutathione content, vitamin C, total protein and albumin levels. However, there was a significant increase in serum ALT and AST activities, lipid peroxides, sialic acid, nitric oxide, serum and hepatic total LDH activities. On the other hand, groups treated with L-carnitine or/and CoQ10 prior to CCl(4) injection showed an improvement in most parameters when compared with cirrhotic control group. It has been concluded that L-carnitine and coenzyme Q10 have a pronounced prophylactic effect against liver damage induced by halogenated alkanes such as carbon tetrachloride.     

红花黄色素滴眼液对大鼠光化学损伤后视网膜变性的保护作用

目的 探讨红花黄色素是否对大鼠光化学损伤引起的视网膜变性有保护作用.方法 选取48只健康SD大鼠并将其随机分为三组：A组为正常对照组、B组为光化学损伤模型组、C组为红花黄色素给药组.B组和C组大鼠在（1900.0±106.9） Lux绿色荧光灯下持续光照射24 h,建立大鼠视网膜光化学损伤模型,分别滴用溶剂对照液、红花黄色素滴眼液.在造模后第6小时、6天、14天,测定视网膜组织中的超氧化物歧化酶（SOD）活性以及丙二醛（MDA）含量,同时,造模后每隔7天对视网膜进行光学显微镜和透视电子显微镜的组织学观察.结果 光照后6d、14 d,红花黄色素滴眼液组视网膜中SOD活性高于模型对照组（P＜0.05）,MDA含量低于模型对照组（P＜0.05）;并且光照后7d,三组视网膜形态结构差异均有统计学意义（（P＜0.05））,红花黄色素滴眼液组病理组织学损害较模型组明显减轻.结论 红花黄色素滴眼液对视网膜光化学损伤有明显的保护作用.     

The protective effect of C-phycocyanin on paraquat-induced acute lung injury in rats

To investigate the potential protective effect of C-phycocyanin (PC) on paraquat (PQ)-induced acute lung injury, rats were divided into control, PQ-treated and PQ + PC-treated groups. Rats in PQ-treated group were orally administered with 50 mg/kg PQ, and rats in PQ + PC-treated group were intraperitoneally injected with 50 mg/kg PC after administration of PQ. At 8, 24, 48 and 72 h after treatments, GSH-Px and SOD activities, MDA levels in plasma and BALF, HYP, NF-κB, IκB-α and TNF-α contents in lung tissues were measured. The pathological changes in lung were observed. After treatment with PC, the levels of MDA and the relative contents of NF-κB and TNF-α were significantly decreased, the activities of GSH-Px and SOD and the relative contents of IκB-α were significantly increased. The degree of rat lung damage was obviously reduced in PQ + PC-treated group. The results suggested that PC treatment significantly attenuated PQ-induced acute lung injury.