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1.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 33(5): 476-480, 2017 May 08.
Article in Chinese | MEDLINE | ID: mdl-29926597

ABSTRACT

OBJECTIVE: To investigate the lipid metabolic effect and mechanism of water extract of lotus leaves(Traditional Chinese Medicine). METHODS: Isolated SD rat lipid tissues were suspended in organ baths containing Krebs solution, and the effect of lotus leaf water extract on free fatty acids (FFA) release was observed; The experimental obesity rat model was established by feeding them high glucose and fat diets, then the changes of body weight and blood lipid were measured in the model rats after intragastric administration with water extract of lotus leaves for four weeks, and the expressions of peroxisome proliferator-activated receptor gamma (PPAR-γ) and leptin were examined by RT-PCR and immunohistochemical. RESULTS: The ex vivo experiment showed that water extract of lotus leaves effectively promoted the FFA release from isolated lipid tissues. In vivo experiment, similarly to Orlistat, water extract of lotus leaves(60 mg/kg)markedly decreased the body weight and blood lipid of experimental obesity rats(P<0.05), and obviously reduced the expressions of PPAR-γ and leptin(P<0.05). CONCLUSIONS: Water extract of lotus leaves greatly improves the expression of PPAR-γ and leptin, which can promote the lipid mobilization and dissolution, reduce the body weight and blood lipid of adult rats with experimental obesity, therefore is expected to be developed into lipid-lowering diet pills.


Subject(s)
Lipid Metabolism/drug effects , Lotus/chemistry , Obesity , Plant Extracts/pharmacology , Animals , Leptin/metabolism , PPAR gamma/metabolism , Plant Leaves/chemistry , Rats , Rats, Sprague-Dawley , Water
2.
Article in Chinese | MEDLINE | ID: mdl-26827534

ABSTRACT

OBJECTIVE: To extract two kinds of phenols 4-hydroxy-3, 5-dimethoxy-4-(2-oxopropyl) cyclohexa-2, 5-dien-l-one and 6-methoxy-5,7-dihydroxy coumarin (named as I and H compounds respectively) from Ajania salicifolia and to investigate their antioxidation and cytotoxicity to tumors and explore their pro-apoptosis mechanism. METHODS: The antioxidant activities of two compounds were assessed by ABTS and DPPH radical-scavenging assays. Two compounds were evaluated for their cytotoxicity against human chronic myelogenous leukemia (K562) cells using the MIT assay. The expression of NF-kappaB P65 mRNA in K562 apoptotic cells was measured by reverse transcription-polymerase chain reaction (RT-PCR), real-time quantitative PCR. In addition, protein expression levels of the NF-ICB P65, p-Akt, Fas, P-catenina and E-cadherin were also measured by Western blot. RESULTS: (1) We found that compound I displayed significant inoxidizability, while compound II had no obvious antioxidizability. (2) In cytotoxicity experiments, compound I didn't display cytotoxicity while compound H displayed obvious cytotoxicity. (3) Compared with the blank group, the expression of NF-kappaB P65 mRNA in K562 cell after treatment with compound II was obviously up-regulated. (4) Compared with the blank group, the expression levels of NF-kappaB P65, Fas, beta-catenina and E-cadherin were significantly increased in compound II treated groups and it appeared obvious dose-effect relationship between the expression of protein and drug concentration. CONCLUSION: Two phenols have obvious antioxidizability and cytotoxicity respectively. On the one hand, the tumor-suppressing mechanism of compound II maybe act by up-regulation the expression of NF-kappaB P65 and Fas protein; thereby, affecting the classical Fas apoptosis signaling pathways. On the other hand, it can also up-regulate the expression of protein beta-catenin and E-cadherin, which participate in the adhesion between cells, and accordingly, playing an important role in preventing the proliferation and metastasis of cancer cells.


Subject(s)
Apoptosis , Asteraceae/chemistry , Phenols/chemistry , Signal Transduction , Antigens, CD , Cadherins/metabolism , Humans , K562 Cells , Oncogene Protein v-akt/metabolism , Transcription Factor RelA/metabolism , Up-Regulation , beta Catenin/metabolism , fas Receptor/metabolism
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