| Cynanchum komarovii Al.Iljinski is a plant belonging to Asclepiadaceae family, distributes widely in the grassland of northern China, and has been used for preventing and reducing inflammation as a traditional Chinese medicine. The phytochemical screening for C komarovii plants revealed a number of bioactive constituents, including alkaloids, flavonoids, polysaccharide, terpenes, fatty acid, phospholipids, amino acids and vitamin. Researchers have been identified thirteen types of alkaloids from C. komarovii. Thereforeour present study aimed firstly on investigating methods of extracting crude alkaloids from these plants, secondly investigating the effects of whole plants on rabbit; thirdly determine the effects of TMPD that represents one of alkaloids of C. komarovii plants on rats for reaching to complete visualization about the effects of these plants on grassland animals.Results of extraction of alkaloids from C komarovii plants showed the extracting yield was2.3g alkaloids for each1kg of plants and this represent high quantity that we reach for it in our study.In the second part of the work, the leaves and roots of C komarovii plants were fed for male and female rabbits in different concentrations (12.5,25.0and50.0%) for two weeks. Mortality, clinical sings, body weight changes, food consumption changes, hematological and biochemical parameters and histological marker were monitored during the study. The results showed locomotor disturbance, loss of appetite; body weight decreasing and death of some rabbits were observed in all treated groups, these signs were accompanied by leukocytosis, anemia and increase in liver and kidney enzymes and decrease in albumin level. The histopathological examination for male and female rabbit’s organ demonstrated presence of periportal septal fibrosis with proliferations and congestion of bile ducts in the liver, dilated and vacuolated cortical tubules of the kidney and degenerative vacuolated myocardial muscle cells. There are dilated alveoli in some areas of the lung and the lesion in spleen represented just in high dose deposition of hemosiderin laden macrophage in red pulp.In the third part, ninety of adult male and female albino rats were randomly into two main groups for investigates the effects of times and dosage of TMPD on rats biochemical and histological parameters. Main group1contains40rats, divided into4 groups, each of10rats. Group1treated with distlled water and serves as control groups, while2,3and4orally were treated with TMPD at77,154.8and231.8mg/kg body weight, respectively for one week.The second main group2contains50rats, also divided into4groups. G1contain20rats serves as control groups while2,3and4contain10rats each, and treated with TMPD half of first dose at38.5,77and115.5mg/kg body weight, respectively for two weeks. In addition to that, six animals from control animals, six from animals administered by231.8mg/.kg body weight and six from animals administered115.5mg/.kg body weight were selected for studies the effects of TMPD on expression some genes that responsible about induced apoptosis in cells. Samples from liver and kidney were directly collected after killing the animals, and placed in cleaned plastic sacks and stored at-80℃until further analysis.Treated animals developed sings of toxicity as weakness, decreas food consumptions, tremors in legs and death. These sings appears after one weeks in treated animals with77,154.8and231.8with death3,3,2animals respectively while the groups that treated by38.5,77,115.5TMPD, sings and death3,2,2animals appeared after12days of treatments. Results of effects TMPD on weights of rats revealed there are no significant differences on weight loss. Results of biochemical tests showed that TMPD causes elevation on liver, kidney and heart enzymes in all treated animals except the value of APL was not significant statistically. On the other hand, the results supplied an explanation more significant increase in enzymes value of treated animals for two weeks and this related to long period of treatments. Hematological tests showed there is significant elevation in WBC, Neut%, Mono%and Lymph%, besides significant decrease in RBC account components that means the animals suffering from anemia.Histological examination for treated rats with TMPD displayed severe renal cortical tubules dilatation in addition to areas of tubular necrosis that shown in high dose treated animals for one week. While the kidney of other treated groups having vacuolated cortical tubules without necrosis, moreover glomeruli seemed unaffected in all treated groups.Histological examinations for liver cells revealed degenerative vacuolation of central hepatocytes, similarly histological examination for heart cells revealed degenerative vacuolation of myocardial cells as.The lung appears very bronchial lymphoid tissues and emphysema in alveoli of high dose treated animals for one and two weeks while treated animals by154.8mg/kg appeared to having emphysema in alveoli and disappear the lesions on other treated groups. The examination for rat’s brain revealed that TMPD doesn’t affects on brain of rats.Results of molecular tests showed TMPD treatment increase expression of Fas-associated death domin protein (FADD) that in turn activated caspases8and pro-caspase3, destruction mitochondria integrity and activated mitochondria-mediated pathway, followed by the release of cyto c and reducing ATP levels. Moreover, TMPD treatment inhibited Bcl2expression and promoted bcl211(Bcl-XL) translocation.In conclusions, alkaloid from C.komaroviithat was extracted by the method of acid-water-alcohol mixtures had reached for a higher extraction yield about2.3g from each1kg of plant, in addition to that the effects of Cynanchumkomarovii plants on animals more influential in contrast to TMPD effects and can lead for singnificant weight loss and increase ALP enzymes in blood and occurance of septal fibrosis in the liver cells with bile ducts proliferation and fibrosis that can progress for liver cancer. Other effects for TMPD alkaloids were promoted apoptosis in liver and kidney cells through activation of mitochondria-mediated caspase-dependent pathway. |
PDF Full Text Request