ABSTRACT
Objective: To investigate the antioxidative activity of compound Astragalus, Glycyrrhiza and Schisandra extract(CAGSE)and determine the content of related bioactive components. Methods: The CAGSE was prepared by the extraction of the Astragalus, Glycyrrhiza and Schisandra raw materials with ethanol. Experimental groups for the antioxidative activity test were set as the control group, vitamin C group(VC group, positive control)and the CAGSE 0.1, 0.2 and 0.5 g/ml groups. The antioxidant effect of CAGSE was evaluated by the assay for the inhibition of linoleic acid autooxidation, the reducing power assay(the method of Oyaizu)and the assay for the 1, 1-diphenyl-2-picryl hydrazine(DPPH)free radical scavenging activity. The content of schisandrae b was determined by the HPLC method, the total phenol content(TPC)was determined by the folin-ciocalteu method using gallic acid as the standard, and the total flavonoid content(TFC)was determined by the ultraviolet spectrophotometry with rutin as the standard. Results :Com- pared with the VC group, the inhibition rate on the linoleic acid autooxidation was significantly increased in all of the CAGSE 0.1, 0.2, and 0.5 g/ml groups(P<0.05)and the reducing power was also significantly enhanced in all the CAGSE groups(P<0.05). The DPPH free radical scavenging activity was significantly higher in the CAGSE 0.1, 0.2 and 0.5 g/ml groups than in the VC group(P<0.05). The TFC in the 0.1 g/ml concentration CAGSE was 54.39 mg/g, the TPC was 38.65 mg/g, and the content of schisandrin b was 0.76 mg/g. Conclusions: The CAGSE showed a significant antioxidant activity, and the content of total flavonoids, total phenolics and schisandrin b were 54.39, 38.65 and 0.76 mg/g, respectively.
ABSTRACT
Carcinogenic test is an important part of non-clinical safety evaluation of new drugs, which aims to evaluate and predict the human carcinogenic risk in long-term drug use by examining the potential carcinogenic effects of drugs on animals. Historical control data may be vital in the interpretation of rare tumors and unexpected increases or decreases of tumors in treated animals compared to controls. Foreign institutions have accumulated a considerable amount of historical control data that can be attributed to the pathological working group and peer review. Such data is valuable and referable, and can be used as a reliable comparator for concurrent study-specific control data. Different experimental animal strains have evolved in history from the F344 rat and B6C3F1 mice, which were traditionally employed by the National Toxicology Program (NTP), to the SD rats, CD-1 mice, and Wistar rats that were routinely used by industrial firms, and finally to the strains of the p53+/- and Tg.rasH2 transgenic mice. It is true that each strain of rodent animal used in carcinogenicity test has different characters in tumorigenesis. Carcinogenicity tests are increasing in China, but the background data that can be referred to is limited so that how to accumulate and use our own historical control data has become challenging. This article summarizes and compares the tumor lesion data of the collected rodent animals, and concludes that different strains have specific types of tumors with gender-related difference.
ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of Schisandra chinensis lignans (SCL) on neuronal apoptosis and PI3K/AKT signaling pathway of rats in the cerebral ischemia injury model, and study its possible mechanism.</p><p><b>METHOD</b>Rats were orally administered SCL high, middle and low dose groups (100, 50, 25 mg x kg(-1)) for 14 days. The cerebral ischemia injury model was established by using the suture-occluded method to rate the neurological functions. The cerebral infarction area was observed by TTC staining. The pathological changes in brain tissues were determined by HE staining. Bcl-2 and Bax expressions were detected by immunohistochemical assay. The protein expressions of p-AKT and AKT were assayed by Western blotting.</p><p><b>RESULT</b>Compared with the model group, SCL high, middle and low dose groups showed reduction in the cerebral infarction area to varying degrees, improve the pathological changes in brain tissues, promote the expression of apoptin Bcl-2 and p-AKT, and inhibit the expression of apoptin Bax.</p><p><b>CONCLUSION</b>SCL shows a protective effect on rats with cerebral ischemia injury. Its mechanism may be related to the increase in p-AKT ability and antiischemic brain injury capacity and the inhibition of nerve cells.</p>