人参果花青素对对乙酰氨基酚致小鼠肝损伤的保护作用

目的探讨人参果花青素(ginseng fruit anthocyanins,GFA)对对乙酰氨基酚(acetaminophen,AP)致小鼠急性肝损伤的保护作用及其机制。方法建立AP诱导的肝损伤模型,观察GFA对肝损伤的保护作用。将ICR小鼠随机分为对照组、模型组(AP 250 mg/kg)和GFA低、高剂量(200、400 mg/kg)组。通过计算脏器指数,检测血清中的丙氨酸转移酶(ALT)、天冬氨酸转移酶(AST)及肝组织匀浆中的丙二醛(MDA)、谷胱甘肽(GSH)水平,结合肝组织切片来观察病理学变化。结果与模型组相比,GFA低、高剂量明显抑制了血清中ALT、AST和匀浆中MDA水平的升高,同时缓解了肝组织匀浆中GSH水平的降低(P0.05);组织病理学HE和Hoechst 33258染色显示GFA可明显改善肝组织的坏死和凋亡,并且缩小了坏死区域,减轻了细胞炎性浸润;通过炎症因子诱导型一氧化氮合酶(i NOS)、环氧化酶-2(COX-2)免疫组织化学染色和硝化应激指标3-硝基络氨酸(3-NT)免疫荧光的表达,说明GFA能够抑制硝化应激和炎症反应。结论 GFA对AP诱导的急性肝损伤有一定的保护作用,其机制可能与其抗氧化作用、抑制硝化应激、减少炎症反应及抑制细胞凋亡有关。     

Protective effect of Lygodium flexuosum (L.) Sw. (Lygodiaceae) against D-galactosamine induced liver injury in rats

The protective effect of Lygodium flexuosum n-hexane extract against D-galactosamine was evaluated in Wistar rats. In preventive groups extract was administered at 48, 24 and 2h before D-galactosamine intoxication whereas in post-treatment groups extract were administered 2, 24 and 48 h after D-galactosamine intoxication. Rats pre-treated with n-hexane extract at a dose of 200 and 100 mg/kg of Lygodium flexuosum showed a significant prevention of elevated AST, ALT, LDH levels and hepatic malondialdehyde in D-galactosamine treated rats. Hepatic glutathione levels significantly upregulated by the extract treatment in D-galactosamine treated rats. Quantification of histopathological sections supported the preventive action of n-hexane extract of Lygodium flexuosum. Rats treated with the extract at a dose of 200 and 100 mg/kg Lygodium flexuosum after the establishment of D-galactosamine induced liver injury showed complete protection of liver as evidenced from normal AST, ALT and LDH levels, hepatic GSH and MDA levels and also by normal histological index of liver in treated rats. Rats treated with n-hexane extract of Lygodium flexuosum were comparable to that of Silymarin, the standard hepatoprotective drug.     

Protective effect of Lygodium flexuosum (L.) Sw. extract against carbon tetrachloride-induced acute liver injury in rats

The hepatoprotective potential of Lygodium flexuosum (L.) Sw. was evaluated in male Wistar rats against carbon tetrachloride-induced liver damage in preventive and curative models. Toxic control and n-hexane extract-treated rats received a single dose of CCl4 (150 microL/100g, 1:1 in corn oil). Pre-treated rats were given n-hexane extracts at 200 and 100 mg/kg dose 48, 24 and 2 h prior to CCl4 administration. In post-treatment groups, rats were treated with n-hexane extract at a dose of 200 and 100 mg/kg, 2, 24 and 48 h after CCl4 intoxication. Rats pre-treated with Lygodium flexuosum remarkably prevented the elevation of serum AST, ALT, LDH and liver lipid peroxides in CCl4-treated rats. Rats treated with the extract after the establishment of CCl4 induced liver injury showed significant (p < or = 0.05) protection of liver as evidenced from normal AST, ALT, LDH and MDA levels. Hepatic glutathione levels were significantly (p < or = 0.05) increased by the treatment with the extracts in both the experimental groups. Histopathological changes induced by CCl4 were also significantly (p < or = 0.05) reduced by the extract treatment in preventive and curative groups. Phytochemical studies revealed the presence of saponins, triterpenes, sterols and bitter principles in Lygodium flexuosumn-hexane extract which could be responsible for the possible hepatoprotective action.     

保肝合剂对急性免疫性肝损伤小鼠的保护作用

目的研究保肝合剂(柴胡、黄芩、法半夏,等)对刀豆蛋白A(Con A)诱导的小鼠急性免疫性肝损伤的保护作用。方法将72只C57BL/6J小鼠随机分为6组:正常组,模型组,保肝合剂低、中、高剂量组(22.5、45、90 mg/kg)和联苯双酯组(100 mg/kg)。每日灌胃(ig)给予小鼠不同剂量保肝合剂14 d后,末次ig后除正常组外,各组均采用尾静脉注射Con A 20 mg/kg制备急性免疫性肝损伤模型。8 h后称重,处死小鼠;检测小鼠血清中丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)及肝组织匀浆中肿瘤坏死因子-α(TNF-α)、干扰素(IFN-γ)、白介素1(IL-1)、白介素6(IL-6)、超氧化物歧化酶(SOD)、丙二醛(MDA)和鸟氨酸氨基甲酰转移酶(OCT)水平;计算肝、脾指数并同时对肝组织进行病理学检查。结果保肝合剂具有剂量依赖性地降低Con A所致小鼠急性肝损伤血清ALT、AST的升高(P0.05),降低肝匀浆中TNF-α、IFN-γ、IL-1、IL-6、OTC的水平(P0.05)及降低肝、脾系数(P0.05),提高SOD的活性(P0.05),减轻Con A对肝组织的病理损伤程度。结论保肝合剂对Con A所致小鼠急性免疫性肝损伤具有一定的保护作用,其机制可能与增强清除自由基的能力从而抑制脂质过氧化以及减少炎性因子的释放相关。     

蚯蚓活性组分对四氯化碳诱导小鼠内质网应激所致急性肝损伤的保护作用

该研究旨在探讨蚯蚓活性组分(EWAs)对四氯化碳(CCl_4)诱导小鼠内质网应激(ERS)所致急性肝损伤的保护作用。腹腔注射10%CCl_4制备内质网应激所致急性肝损伤模型;血清生化指标检测ALT,AST,SOD,GSH-PX酶活性及MDA含量变化;计算肝、脾指数;HE染色观察肝脏病理学变化;TUNEL法检测肝组织细胞凋亡情况;免疫组织化学法检测ERS标志性蛋白GRP78和CHOP表达情况;Western blot法检测ERS相关蛋白的表达水平。结果显示,与模型组小鼠相比,EWAs的高、中、低剂量组血清学各项指标均有显著改善(P0.05或P0.01),肝脏病变范围减小,且损伤程度明显减轻,小鼠肝脏指数和脾脏指数均有明显变化(P0.05或P0.01);各剂量给药组的肝组织细胞凋亡指数明显下降(P0.05或P0.01);肝组织中ERS相关蛋白GRP78和CHOP表达水平显著降低(P0.05或P0.01),各剂量给药组均能显著下调GRP78和CHOP以及CHOP上游信号通路PERK-eIF2α-ATF4的蛋白表达(P0.05或P0.01)。综上,EWAs对ERS所致的小鼠急性肝损伤具有显著保护作用,其机制可能通过抑制氧化应激和ERS,从而减轻肝脏损伤,并可下调ERS标志性凋亡蛋白CHOP表达,抑制细胞凋亡实现的。     

玉米肽对动物实验性肝损伤的保护作用

玉米肽对四氯化碳和硫代乙酰胺引起的小鼠急性肝损伤具有明显的保护作用 ,抑制血清中谷丙转氨酶活性的升高 ,降低丙二醛含量并增加肝糖原含量 ,对乙硫氨酸引起的小鼠脂肪肝中三酸甘油脂含量也具有明显的降低作用     

维药菊苣对小鼠急性化学性肝损伤的保护作用

目的:观察菊苣乙醇提取物和水提物对四氯化碳所致小鼠急性肝损伤的保护作用。方法:用95%乙醇和蒸馏水对药材进行回流提取,用0.1%四氯化碳橄榄油溶液10m l/kg腹腔注射造模,以血清丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)含量为指标观察对肝损伤的保护作用。结果:菊苣水提物(1.5g/kg、3g/kg、6g/kg)、醇提物(1.6g/kg、3.2g/kg、6.4g/kg)对CC l4所致肝损伤小鼠血清升高的ALT、AST有降低作用。结论:菊苣水提物和乙醇提取物对小鼠四氯化碳所致小鼠急性肝损伤有保护作用。     

Protective effect of Rhinax,a herbal formulation,against CCl4-induced liver injury and survival in rats

Rhinax, a herbal formulation, was investigated for its protective activity against CCl₄-induced liver injury and survival in rats. Oral administration of Rhinax at a dose of 80 mg/kg significantly reduces the hepatotoxic effects of CCl₄. It also significantly improves the survival of rats at a dose of 160 mg/kg. On the basis of these observations, we conclude that Rhinax possesses anti-hepatotoxic activity and that the observed activity may be due to the increased activity of cytochrome P450, thereby exerting an inhibitory effect on reductive pathways of CCl₄.     

金银花总黄酮对小鼠免疫性肝损伤的保护作用

目的:观察金银花总黄酮(Lonicera gaponica total flavone,LJTF)对卡介苗(BCG)联合脂多糖(LPS)所致小鼠免疫性肝损伤的保护作用。方法:采用BCG 2.5mg静脉注射致敏小鼠,d10给于LPS 7.5μg静脉攻击造成小鼠免疫性肝损伤模型,ig给于LJTF(100、200、400mg/kg)连续10天。分光光度法测定血清ALT、AST浓度,肝匀浆中MDA、SOD的含量;免疫组化研究肝脏肿瘤坏死因子-α(TNF-α)和核因子(NF)-κB p65的表达。结果:免疫性肝损伤小鼠血清ALT、AST较正常组明显升高,肝脏中MDA明显升高而SOD较正常组明显降低。LJTF ig能降低免疫性肝损伤小鼠血清中升高的ALT、AST含量,降低肝匀浆中MDA水平,同时升高其低下的SOD水平,LJTF也能降低免疫性肝损伤小鼠TNF-α和NF-κB p65在肝脏中的强烈表达。结论:LJTF对免疫性肝损伤小鼠有保护作用,机制与减少自由基的产生、抑制细胞膜脂质过氧化、减少炎症介质的释放有关。     

穿山龙水提物对四氯化碳致急性肝损伤模型小鼠toll样受体4/髓样分化因子88通路的影响

目的 观察穿山龙水提物对四氯化碳诱导急性肝损伤模型小鼠的影响,探讨其对toll样受体4(Toll-like receptors 4,TLR4)/髓样分化因子88(Myeloid differentiation factor88,MyD88)信号通路的调控作用.方法 60只小鼠按随机数字表法分为对照组,模型组,穿山龙水提物低、中、高剂量组,每组10只.穿山龙水提物低、中、高剂量组分别灌胃50、100、200 mg/kg穿山龙水提物混悬液,对照组和模型组灌胃等体积溶剂.1次/d,连续给药7 d.末次给药后2 h,除对照组外,其余各组小鼠腹腔注射0.35%四氯化碳橄榄油溶液建立急性肝损伤模型.造模后24 h,采用Western blot检测各组肝组织TLR4、MyD88、NF-κB p65表达;采用PCR法检测各组肝组织IL-1β、TNF-α、IL-6 mRNA表达;采用ELISA法检测各组小鼠血清AST、ALT含量.结果 与模型组比较,穿山龙水提物低、中、高剂量组小鼠血清AST[(98.00±17.75)U/L、(57.49±9.66)U/L、(39.60±9.49)U/L比(113.40±9.71)U/L]、ALT[(76.00±14.73)U/L、(50.70±9.35)U/L、(35.25±9.93)U/L比(95.42±11.64)U/L]水平降低(P<0.01);穿山龙水提物高剂量组MyD88[(0.67±0.21)比(1.74±0.42)]、NF-κB p65[(0.51±0.09)比(1.76±0.31)]、TLR4[(0.97±0.25)比(2.99±0.72)]表达降低(P<0.01);穿山龙水提物中、高剂量组IL-6 mRNA[(2.22±0.25)、(1.76±0.31)比(5.20±0.60)]、IL-1βmRNA[(1.96±0.35)、(1.47±0.23)比(7.37±0.99)]、TNF-αmRNA[(2.06±0.25)、(1.34±0.33)比(2.98±0.50)]表达降低(P<0.01).结论 穿山龙水提物通过抑制TLR4/MyD88信号通路实现对四氯化碳诱导小鼠急性肝损伤的保护作用.     

Protective effect of Bojungikki-tang, a traditional herbal formula, against alcohol-induced gastric injury in rats

Ethnopharmacological evidence

Oxidative stress plays an important role in the pathogenesis of ethanol-induced acute gastric mucosal injury. Bojungikki-tang (Hochuekkito in Japanese, Bu-zhong-yi-qi-tang in Chinese) is a traditional herbal formula used in Korea, Japan, and China to treat allergic diseases and gastrointestinal disorders. However, the mechanism responsible for its actions has not been investigated experimentally.

Aim of the study

The aims of this study were to investigate whether Bojungikki-tang water extract (BJITE) has protective effects against ethanol-induced acute gastric injury in rats and to perform an acute toxicity study to evaluate its safety.

Materials and methods

In this rat model, gastric mucosal injury was imposed by oral administration of 5 mL/kg body weight of absolute ethanol. BJITE at one of two doses (200 or 400 mg/kg body weight) was administered by gavage 2 h before ethanol administration. Gastric tissues were collected and analyzed to assess the gastric injury index, and content or activity of catalase, superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione-S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx).

Results

Acute administration of ethanol significantly increased the gastric injury index concomitantly with an increase in MDA and GSH content, and a decrease in the activities of catalase, GST, GR, GPx, and SOD. Pretreatment with 200 or 400 mg/kg BJITE attenuated ethanol-induced gastric mucosal injury; this was accompanied by an increase in the content or activity of PGE₂, catalase, GSH, GST, GR, GPx, and SOD, and a decrease in MDA content. In the acute toxicity study, no adverse effects of BJITE were observed at doses up to 2000 mg/kg body weight.

Conclusion

These results indicate that BJITE can partly protect the gastric mucosa from ethanol-induced acute gastric injury and suggest that these protective effects might be induced by increasing the antioxidant status. We suggest that BJITE can be developed as an effective drug for the treatment of acute gastric injury.     

Protective effect of a polyherbal formulation (Immu-21) against cyclophosphamide-induced mutagenicity in mice

The object was to evaluate the effects of a polyherbal formulation, Immu-21, against cyclophosphamide (CP)-induced chromosomal aberrations (CA) and micronuclei (MN) in mice. CP alone (40 mg/kg, i.p.) produced classical as well as non-classical chromosomal aberrations in mice, and the incidence of CA was significantly more in the CP treated group when compared with that of the control group. Immu-21, which contains extracts of Ocimum sanctum, Withania somnifera, Emblica officinalis and Tinospora cordifolia, was given at 100 mg/kg, daily, over 7 days, and 30 mg/kg daily over 14 days and inhibited both CP-induced classical and non-classical chromosomal aberrations ( approximately 40%-60% of control). A significant increase in MN was also observed in bone marrow erythrocytes of mice treated with CP, and pretreatment with Immu-21 also significantly reduced these. Cytotoxicity was evaluated by estimating the ratio of polychromatic erythrocytes (PCEs) to normochromatic erythrocytes (NCEs). The present results indicate that chronic treatment with Immu-21 prevented CP-induced genotoxicity in mice.     

杠板归总黄酮对抗结核药物致肝损伤小鼠的保护作用及机制研究

目的:研究杠板归总黄酮对抗结核药物致肝损伤小鼠的保护作用,并探索作用机制。方法:将60只小鼠随机分为6组,即正常组、模型组、葡醛内酯组(200 mg/kg)及杠板归总黄酮组(600 mg/kg,300 mg/kg,150 mg/kg)。除正常组外,其余各组均灌胃异烟肼和利福平各100 mg/kg造模,同时给予杠板归总黄酮干预,每天1次。第30天,取血和肝组织,采用生化法检测血清中ALT和AST活性;酶联免疫吸附法(ELISA)检测肝组织TNF-α、IL-1β和IL-6含量;Western Blot检测肝组织Fas表达;HE染色进行肝组织病理学检查。结果:与模型组相比,杠板归总黄酮(600 mg/kg、300mg/kg)能够明显降低肝损伤小鼠血清中ALT和AST活性,明显抑制肝组织TNF-α、IL-1β、IL-6和Fas表达,并改善肝组织病变,而杠板归总黄酮组150 mg/kg对抗结核药物致肝损伤无改善作用。结论:杠板归总黄酮可保护异烟肼和利福平联用导致的肝损伤小鼠,其机制可能与抑制Fas通路和抗炎作用有关。     

长片金线兰多糖对四氯化碳诱导急性肝损伤小鼠的保护作用

目的研究长片金线兰多糖的结构特征以及对四氯化碳(CCl_4)致小鼠急性肝损伤的保护作用。方法从长片金线兰中提取多糖,分析其相对分子质量、单糖组成、紫外与红外吸收特征。将48只ICR小鼠随机分为对照组、模型组、联苯双酯(150 mg/kg)组和长片金线兰多糖低、中、高剂量(100、200、400 mg/kg)组,给予相应药物干预9 d后,除对照组外,其余各组ip CCl_4造成急性肝损伤,16 h后检测各组小鼠血清中丙氨酸转氨酶(alanine aminotransferase,ALT)、天冬氨酸转氨酶(aspartate aminotransferase,AST)和乳酸脱氢酶(lactate dehydrogenase,LDH)活性;测定各组大鼠肝脏组织中超氧化物歧化酶(superoxide dismutase,SOD)、过氧化氢酶(catalase,CAT)活性以及谷胱甘肽(glutathione,GSH)和丙二醛(malondialdehyde,MDA)含量;采用苏木素-伊红(HE)染色法观察各组小鼠肝脏组织病理变化。结果长片金线兰多糖的相对分子质量为4.254×10~5,由甘露糖、鼠李糖、半乳糖醛酸、葡萄糖、半乳糖、木糖和阿拉伯糖组成(物质的量比为1∶0.11∶0.19∶11.15∶0.87∶0.36∶0.18),紫外与红外光谱扫描结果推测其可能为一种吡喃型杂多糖。与模型组比较,长片金线兰多糖能够显著降低CCl_4致肝损伤小鼠血清中ALT、AST和LDH活性(P0.05、0.01),提高肝脏组织中SOD、CAT活性和GSH含量(P0.05、0.01),降低MDA含量(P0.01),减轻CCl_4对肝组织的病理损伤。结论长片金线兰多糖对CCl_4致小鼠急性肝损伤具有一定的保护作用,其机制可能与抑制脂质过氧化有关。     

鸭跖草水提取物对小鼠脑缺血再灌注损伤的保护作用

目的:探讨鸭跖草对小鼠脑缺血再灌注损伤的保护作用。方法:昆明种小鼠65只随机分成假手术组、模型组和鸭跖草水提物高、中、低剂量组。鸭跖草高、中、低剂量组小鼠分别灌服鸭跖草水提物20,10,5g/kg.d,模型组和假手术组小鼠在相同时间点灌服等体积的蒸馏水,连续10d。末次给药1h后,模型组和鸭跖草各剂量组小鼠均采用夹闭双侧颈总动脉30min再灌注60min的方法复制急性脑缺血再灌注损伤模型,假手术组仅做双侧颈总动脉分离术,不夹闭。测定各组小鼠脑指数、脑组织含水量、脑匀浆中丙二醛(MDA)含量及脑组织超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力,并观察大脑皮层和海马CA1区细胞形态的变化。结果:与模型组比较,鸭跖草高、中剂量组小鼠脑指数和脑组织含水量均降低(P<0.01和P<0.05),脑匀浆中MDA含量减少(P<0.01),而SOD和GSH-Px的活力增加(P<0.01和P<0.05),且大脑皮层和海马CA1区神经元损伤减轻。结论:鸭跖草水提物对小鼠脑缺血再灌损伤具有保护作用,其机制与抗氧化作用有关。     

天麻多糖对小鼠免疫性肝损伤的保护作用

目的:研究天麻多糖(polysaccharides from Dabie Mountain Gastrodia elata Bl.PDG)对卡介苗(BCG)加脂多糖(LPS)导致的小鼠免疫性肝损伤的作用。方法:造卡介苗加脂多糖导致小鼠免疫性肝损伤模型,以联苯双酯(bifendate,BF)为阳性对照,测定血清中天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)与一氧化氮(NO),测定肝脏中超氧化物歧化酶(SOD)与丙二醛(MDA),用酶联免疫法来测定血清中和肿瘤坏死因子α(Tumor necrosis factor-α,TNF-α)与白细胞介素-1(Interleukin-1,IL-1)的含量,噻唑蓝(MTT)法来测定脾T、B淋巴细胞增殖能力,称量并分别计算各组肝脏、胸腺与脾脏指数。结果:天麻多糖组(25、50、100mg/kg)能显著降低小鼠血清中ALT、AST、NO活性及TNF-α与IL-1的含量,抑制肝脏中的MDA水平和提高的SOD活性,显著提升脾T、B淋巴细胞增殖能力,且提高了小鼠的脾脏、胸腺指数,降低了肝脏指数。结论:天麻多糖对卡介苗加脂多糖导致小鼠免疫性肝损伤有良好的保护作用。     

Protective effect of gentiopicroside from Gentiana macrophylla Pall. in ethanol‐induced gastric mucosal injury in mice

Gentiopicroside isolated from gentiana macrophylla Pall. belongs to iridoid glycosides. This study aimed to evaluate the protective effect of gentiopicroside against ethanol‐induced gastric mucosal injury in mice. Mice were proactively administrated with gentiopicroside by intragastric administration once a day for 3 consecutive days. On the 3rd day, gastric ulcer in mice was induced with 70% ethanol after the last intragastric administration. The stomach tissues were submitted for evaluation of the severity of gastric mucosal alterations. Gentiopicroside administrated orally ameliorated the severity of gastric mucosal alterations. Oral administration of gentiopicroside significantly increased heat shock protein‐70 and glutathione levels and superoxide dismutase activity, normalized epidermal growth factor and vascular endothelial growth factor levels, and decreased the levels of tumour necrosis factor‐α, interleukin‐6 and malondialdehyde, and myeloperoxidase activity in gastric tissue. These findings demonstrated that gentiopicroside has protective effect against ethanol‐induced gastric mucosal injury in mice through the improvements of antioxidative and anti‐inflammatory effects, as well as up‐regulation of heat shock protein‐70 level and normalization of epidermal growth factor and vascular endothelial growth factor levels. The results presented in this study provide some evidence for the development of a novel antigastric ulcer agent.     

打箭菊对D-半乳糖胺所致大鼠急性肝损伤的保护作用

目的:研究藏药打箭菊对D-半乳糖胺(D-galactosamine,D-Gal)所致大鼠急性肝损伤的保护作用。方法:60只大鼠随机分为正常对照组、模型组、高中低剂量给药组、阳性对照组等6个组。给药组按18 g/kg、9 g/kg、4.5 g/kg剂量以打箭菊水提物灌胃;阳性对照组按50 mg/kg联苯双酯灌胃,每天1次,共7天。灌胃给药第6天下午,模型组和给药组按500 mg/kg体重腹腔注射D-Gal一次。第8天,末次给药24 h(腹腔注射36 h)后,测定血清生化指标,并测体重和肝脏重、脾重、胸腺重,求脏器系数,同时切取肝脏检测肝糖原,取肝组织作病理观察。结果:打箭菊18 g/kg、9 g/kg、4.5 g/kg剂量给药组均可显著降低急性肝损伤大鼠血清ALT、AST、ALP水平和TBA、T-Bil含量,促进血清中TP、ALB和肝组织中肝糖原的增加,且中低剂量给药组对肝重量增大和胸腺萎缩有抑制作用。病理检查结果也显示有明显的保肝作用。结论:打箭菊对D-Gal所致大鼠急性肝损伤有保护作用,其作用机制与多环节有关。     

Protective effect of a Butea monosperma (Lam.) Taub. flowers extract against skin inflammation: Antioxidant,anti-inflammatory and matrix metalloproteinases inhibitory activities

Ethnopharmacological relevance

Butea monosperma (Lam.) Taubert (Syn. Butea frondosa; family Fabaceae) is a common plant of the Indian continent ( 13 and 44). The brightly orange flowers of this plant are widely used in traditional medicine and more particularly for inflammatory disease.

Aim of the study

In vitro anti-inflammatory mechanism of a hydroethanolic extract of B. monosperma flowers (BME) and more specifically of an enriched fraction in butrin and isobutrin (BI) was studied using cell culture of Normal Human Keratinocyte, cells involved in the skin inflammatory.

Materials and methods

Dried and crushed B. monosperma flowers were extracted with Ethanol/H₂O (70/30 v/v). The butrin/isobutrin fraction was obtained by centrifugal Partition Chromatography (CPC). Experiments were conducted on UV-B treated normal human epidermis keratinocytes, cells involved in the skin inflammatory response. To evaluate extract anti-inflammatory activity, cytokines IL-1β, IL-6, IL-8, prostaglandin E₂ and metalloproteinases MMP-1, -2, -9 and -10 were measured in the cells supernatant.

Results

Our data clearly showed that hydroalcoholic B. monosperma flower extract was able to decrease the secretion of IL-1β, IL-6 and IL-8 pro-inflammatory cytokines of -32, −33 and -18% respectively. Interestingly, Prostaglandin E₂ production and the secretion of MMP-1, -2, -9 and -10 were also inhibited. Same results were observed in presence of enriched fraction in butrin and isobutrin and confirmed the participation of these molecules in the anti-inflammatory activity.

Conclusion

These results explain the anti-inflammatory activity of B. monosperma and confirm the interest to use it in traditional Indian medicine. Moreover, its metalloproteinases inhibitory activities coupled with its anti-inflammatory action also give anti-aging property to this plant.     

Protective effect of Calamintha officinalis Moench leaves against alcohol-induced gastric mucosa injury in rats. Macroscopic, histologic and phytochemical analysis

Calamintha officinalis Moench (Lamiaceae) is an aromatic plant used since ancient times for its preservative and medicinal properties. The plant, known as 'Mentuccia' in Central Italy, is used in cooking as an aromatizant and to impart aroma and flavour to food. The methanol extract of the leaves was subjected to phytochemical and biological investigations. The extract contains polyphenols, catechic tannins and terpenes and shows radical scavenger activity. By means of HPLC analysis, eriocitrin, eriodyctiol, acacetin, linarin, benzoic acid and some phenolic acids, such as caffeic, chlorogenic, p-coumaric, were determined. The gastroprotective activity of the extract was investigated using ethanol-induced ulcer in rats, with sucralfate as a reference drug. Samples of gastric mucosa, stained by PAS and haematoxylin/eosin, were observed by light microscopy. The efficacy of the extract was comparable to that of the reference drug. Probably the gastroprotective effect depends on a synergistic action of all the compounds occurring in C. officinalis leaves, even if the antioxidant potential of the leaves plays an important role by removing damaging agents from the gastric mucosa.