Study on chemical composition of essential oil and anti-oxidant and anti microbial properties of Artemisia haussknechtii

Artemisia species with common Persian name of Dermaneh are found all over Iran and are used for treatment in infectious diseases such as malaria, hepatitis and other diseases. Some Artemisia species are used in traditionally as tonic and anti-helmintic in north of Iran. The aim of this study was to investigate chemical composition of the essential oil of Artemisia haussknechtii. Also potential antioxidant and anti microbial activities of the essential oil and ethanolic extract were studied. The essential oil was prepared by hydrodistillation and analyzed by GC and GC/MS instruments. Antioxidant activity was evaluated by methods; namely DPPH, free radical scavenging, FTC system and total phenolic compounds analyzing. The antimicrobial activities of the extract were individually tested against a panel of microorganisms using disc diffusion method and MIC [minimum inhibitory concentration] measurement. Forty-eight components were identified constituting 98.35 of total oil. Camphor [12.4%], alpha-Terpineol [9.93%], Davana ether [6/24%], and Bornyl acetate [3.77%] were the major components. Good antioxidant activity of extract; increasing with the increment of concentration of plant extract was revealed. Ethanolic extract of Artemisia haussknechtii inhibited both gram-positive and gram-negative bacteria. MIC of the extract against yeast was the lowest [2.5 micro sign g/ml]. A known anti-bacterial compound [camphor] was one of major components in the essential oil, ethanolic extract showed good anti-oxidant activity and also extract inhibited growth of both gram positive and gram negative bacteria and fungi. These findings supported some traditional use of this plant

Effect of silymarin mixed with Dimethyl Dimethoxy Biphenyl Dicarboxylate versus silmarin alone in liver of rats treated with carbon Tetrachloride

This study aimed to investigate the effect of a combination of silymarin and dimethyl dimethoxy biphenyl dicarboxylate [Mepacure] versus silymarin alone on the development of acute hepatic injury caused in the rat by the administration of CCLi in vivo. Mepacure at doses of 8.4, 16.8 and 25.2 mg/kg containing mixture of silymarin at doses of 5.2, 10.4 or 15.6 mg/kg and dimethyl dimethoxy biphenyl dicarboxylate [DDP] at doses of 3.2, 6.4 or 9.6 mg/kg, respectively, or silymarin alone at a dose of 22 mg/kg were given once daily orally simultaneously with CCU and for 15 days thereafter. Liver damage was assessed by determining serum enzyme activity and hepatic histopathology. Stained sections were subjected to morphometric evaluation using computerised image analyzer. The combination of silymarin and DDP administered to CCL4 treated rats at the above doses, resulted in a dose-dependent decrease of elevated alanine aminotransferease [ALT] by 27.5, 30 and 35%, aspartate aminotransferase [AST] by 10.3, 34.7 and 45% and alkaline phosphatase [ALP] levels by 10.8, 15.7 and 33.4%, respectively. Meanwhile, silymarin administered alone, reduced the elevated ALT, AST and ALP levels by 28, 39.4 and 14.2%, respectively. Total proteins in serum were reduced in CCL4 treated rats by 33.3% compared with normal rats. In CCL4 treated rats, proteins in serum increased after the combination of silymarin and DDP by 16.4-18.8%. Meanwhile, silymarin alone increased serum proteins by 27% compared with CCL4 treated control rats. Histological examination of liver specimens revealed a marked reduction in liver cell necrosis in rats treated with the combination of silymarin and DDP or with silymarin alone compared with CCL4 rtreated control rats. Quantitative analysis of the area of damage showed a 93.8% reduction in the area of damage in CCL4 treated rats after treatment with silymarin alone and 56.3, 72.8 and 81.3% reduction after the combination of silymarin [5.2, 10.4 or 15.6 mg/kg] and DDP [3.2, 6.4 or 9.6 mg/kg], respectively. Data in the present study indicates that DDP potentiates the protective effect of silymarin on hepatic injury caused by CCL4 in rats