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Tumor has become one of the major diseases threatening human health at present. Conventional therapies for tumor have serious side effects and are prone to drug resistance， while new therapies are expensive and impose a heavy burden on patients. Chinese herbs effective in the treatment of tumor contain a variety of natural active ingredients， and many anti-tumor drugs used in clinical practice are derived from Chinese herbs. Polysaccharides， ubiquitous in Chinese herbs， are easy to extract and have antitumor， antiviral， and antioxidant activities. Studies have demonstrated that the polysaccharides from Chinese herbs have significant anti-tumor effect and are characterized by multi-target and multi-mechanism functioning， which can avoid the development of drug resistance， exhibiting a great research value and the potential to be developed into novel anti-tumor drugs. Their anti-tumor mechanisms mainly include the inhibition of tumor proliferation， promotion of apoptosis， induction of autophagy， influence on cell cycle， inhibition of tumor angiogenesis， modulation of epithelial-mesenchymal transition （EMT） and immunity， promotion of tumor oxidative stress， and regulation of phosphatidylinositol 3-kinase/ protein kinase B （PI3K/Akt）， Toll-like receptor 4 （TLR4）， mitogen-activated protein kinase/nuclear factor-kappa B （MAPK/NF-κB）， adenosine 5'-monophosphate （AMP）-activated protein kinase/mechanistic target of rapamycin （AMPK/mTOR）， epidermal growth factor receptor/extracellular signal-regulated kinase （EGFR/ERK）， p53， and Wnt/β-catenin signaling pathways.
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Objective To explore the effect of continuous hyperglycemia on learning and memory capacity in rats, and to observe the changes of expressions of ubiquitin and apotosis-related proteins, so as to provide a relative basis for diabetic encephalopathy. Methods The male SD rats were randomly divided into normal control group and diabetes mellitus (DM) group. The DM rats was made by intraperitoneal injection of streptozocin (STZ). The capacities of learning and memory were tested by Y-maze. The structure changes in frontal lobe cortex and hippocampus were observed by Nissl's staining and immunohistochemistry. The apoptosis cell count was measured by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The expressions of Bcl-2 and P53 were assessed by Western-blot analysis. The expression of ubiquitin mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). Results In DM rats, the learning and memory capacities were worse than in control rats (P＜0. 05), and the apoptosis cell counts in frontal lobe cortex and hippocampus were higher than in control rats, the expression of Bcl-2 gene was reduced while the expressions of ubiquitin and P53 gene were increased (P＜0. 05). Conclusions In the frontal lobe cortex and hippocampus, the expression of Bcl-2 gene is reduced while the apoptosis cell numbers and ubiquitin P53 gene expression are increased, which may contribute to neurodegeneration in DM rats.
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Aim To investigate the effects of anisodamine on the pressure of portal vein of experimental liver fibrosis and its mechanisms of action. Methods The experimental liver fibrosis model was produced by CCl_4. The preventive group was treated ten weeks with anisodamine 7.0 mg?kg~(-1) ip once everyday. All therapeutic groups were treated six weeks with anisodamine 7.0 mg?kg~(-1) or 14.0mg?kg~(-1) ip once everyday. After CCl_4 injection for ten weeks, the pressure of portal vein,the content of NO in livers, and liver iNOS and eNOS mRNA expressions were detected with different methods.Results The pressure of portal vein was significantly reduced in anisodamine preventive group and anisodamine therapeutic groups. The liver content of NO and the expression of iNOS and eNOS were all inhibited by the treatment of anisodamine.Conclusion Anisodamine reduced the expressions of iNOS and eNOS to synthesis of NO in liver. As a result, the pressure of portal vein of fibrosis rats decreased. So Portal hypertension of liver fibrosis may be improved by anisodamine in patients.
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Objective To investigate the protective effects and the mechanisms of anisodamine on experimental liver damage. Methods The experimental liver injury model was established by ANIT and CCl 4.Studies were made after ANIT or CCl 4 administration,and the control group compared with the experimental groups which were treated by anisodamine on the pathologic morphology, biochemical indices and the contents of Ca 2+ ,MDA and the ability of total antioxidation in the liver.Effects of anisodamine on sleeping time of the mice toxicated by given sodium phenobarbital were also determined.Results The elevation of ALT, ALP, BiL, CHE and the decrease of serum protein in ANIT or CCl 4 liver damage were significantly improved by treatment with anisodamine .It also remarkably diminished the hepato-cellular and chole-epthelial-cellular degeneration and necrosis induced by ANIT or CCl 4.The contents of Ca 2+ ,MDA and the ability of total antioxidation in the liver were all decreased by treatment with anisodamine. The sleeping time induced by sodium phenobarbital in the toxicated mice was reduced by anisodamine. Conclusion Anisodamine have significant protective effects on liver injury of intrahepatic cholestasis and chemical hepatitis and the mechanism may be associated with blocking M-receptor and enhancing antioxidation and antitoxic activity in liver.
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AIM : To observe the effects of naoyikang on the capability of learning and memory in Alzheimer’s disease model mice. METHODS : The mice model was established by intraperitoneal injection of D BZ Gal and NaNO 2, the capability of learning and memory was tested on mice by electrical maze and water maze, the levels of superoxide dismutase (SOD) and malondialdehyde(MDA) of brain tissues were assayed by biochemical methods,and the changes in ultrastructure were observed by Transmission Electron Microscope. RESULTS : The capability of learning and memory of model mice decreased and the level of SOD of model mice decreased and MDA increased. Compared with the madel group, they were obviously improved in low, middle and high doses ( 2.4 , 7.2 , 24 g?kg -1 ?d -1 ) of naoyikang group ([WTBX P
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AIM: To observe the protective effect of naoyikang-containing serum on cultured hippocampus neuron injury induced by D-galactose(D-gal).METHODS: Naoyikang-containing serum was prepared in rats administered with aqueous extract of naoyikang(6.84 g?kg-1?d-1).MTT,MAO-B and ATPase assay were used to measure the viability of hippocampus neurons.RESULTS: D-gal at concentration of 100 ?mol/L caused significant decrease in the viability of hippocampus neurons 24 h after the treatment.Naoyikang-containing serum increased the viability,ATPase activity and the expression of bcl-xl mRNA,decreased the MAO-B activity and the expression of bax mRNA in D-gal injured hippocampus neurons.CONCLUSION: Naoyikang-containing serum prevents hippocampus neurons from D-gal induced cytotoxicity.