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Objective To study the in situ intestinal absorption behaviors of 3,29-dibenzoyl-karounitriol(DK)in Gualou-Xiebai(GX)extract in rats. Methods A rat in situ single-pass perfusion model was used and the concentrations of the perfusate were determined by HPLC-PDAD to investigate the intestinal absorption site and mechanism. Results The main absorption site of DK in GX extract was jejunum,ileum and colon,and the absorption had no significant difference in the three different segments of rat intes?tine(P>0.05),but was significantly higher than that in duodenum(P0.05). Conclusion DK in GX extract could be absorbed in whole intestinal segment,with the best intestinal absorption site of jejunum,ileum and colon. Its absorbing mechanism may be related to passive diffusion.
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Objective To verify the protective effects of Gualou Xiebai dropping pills(GX)on myocardial ischemia-reperfu?sion injury(MIRI)in rats. Methods After screening the qualified SPF rats were randomly divided into four groups,with 12 in each group. Sham-operated group and model group rats were respectively treated with normal saline,and rats in GX group and compound Danshen dropping pills group were given the corresponding dropping pills equivalent to 22.5 g/kg and 85.05 mg/kg of the crude herb,re?spectively. All groups were administered once a day for 7 successive days. One hour after the last administration,the MIRI models were produced by occluding the left coronary artery for 30 min and releasing the occlusion for 120 min. The changes in ST segment were observed,and the contents of creatine kinase-MB(CK-MB),cardiac troponin-T(CTNT)and myoglobin(MYO)in blood plas?ma were measured. The pathological changes in myocardial tissues were observed by optics and electric-microscope and the percentage of myocardial infarction was measured by detecting the content of Evan blue in myocardium. Results Compared to normal saline in the model group,GX had antagonism to ECG S-T segments elevation in rats with myocardial ischemia,while the contents of CK-MB, MYO,and CTNT in blood plasma declined significantly(P<0.05 or P<0.01);the disorder condition of myocardial cell fiber arrange?ment was improved,and edema between myocardial tissue and cells was relieved;the inflammatory cell infiltration and myocardial ne?crosis in cardiac allograft were significantly alleviated,and the percentage of myocardial infarction was decreased significantly(P<0.01). Conclusion GX may play an important protective role against the MIRI in rats.
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Aim To study the interfering effects of picrosideⅡ on the expressions of nuclear transcription factor kappaB(NF-κB)and inhibitor of NF-κB(I-κB)after cerebral ischemic reperfusion in rats.Methods Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion models in rats.PicrosideⅡ(10 mg·kg~(-1))and salvianic acid A sodium(10 mg·kg~(-1))were injected from the tail vein for treatment.TUNEL positive cells were counted by immunofluorescence assay.The expressions of NF-κB and I-κB were determined by immunohistochemical assay,and the concentration of NF-κB and I-κB in brain tissue was determined by ELISA.Results The exprssions of NF-κB and I-κB were weakly and the apoptotic cells were scattering at cortex,striatum and hippocampus in the sham operative group.In the negative control group,the number of TUNEL positive cells and the expressions of NF-κB and I-κB increased,the absorption(A)values and the concentration were significantly higher than those in the sham operative group(P<0.05).While in the positive control and picroside groups,the expressions(A values)and concentration of NF-κB and I-κB and the number of TUNEL positive cells were significantly lower than those in the negative control group(P<0.05).There was no significant difference between the positive control group and picroside group(P>0.05).Conclusion Picroside Ⅱ might downregulate the expressions of NF-κB and I-κB to inhibit neuronal apoptosis induced by inflammation after cerebral ischemia reperfusion injury in rats.
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Aim To explore the effect of picrodideⅡ on the expressions of Caspase-3 and poly ADP-ribose polymerase (PARP) in brain tissue following cerebral ischemic reperfusion injury in rats.Methods The middle cerebral artery occlusion reperfusion models were established with intraluminal thread methods in rats. PicrodideⅡ (10 mg·kg~(-1)) and salvianic acid A sodium (10 mg·kg~(-1)) were injected from tail vein for treatment. The neurological function was evaluated with Bederson's test and the cerebral infarction volume was observed with tetrazolium chloride (TTC) staining.The brain structure was observed by hematoxylin-eosin (HE) staining and the apoptosis was counted by TUNEL immunofluorescence assay. The expressions of Caspase-3 and PARP were detected with immunohistochemical and enzyme linked immunosorbent assay.Results After ischemia 2 h and reperfusion 22 h, the rats showed neurological function deficit and cerebral infarction in ischemic hemisphere. The expressions of Caspase-3 and PARP and the number of apoptotic cells in brain tissue increased compared with those in the sham operative group (P <0.05). In picroside and salvianic acid A sodium groups, the Bederson's scores and cerebral infarction volume, the expressions of Caspase-3 and PARP and the number of apoptosis cells were lower than those in the negative control group (P <0.05). While there was no significant difference in five indexes metioned above between picroside group and salvianic acid A sodium group (P >0.05).Conclusion PicrosideⅡ might reduce the expressions of Caspase-3 and PARP to inhibit the neuronal apoptosis induced by cerebral ischemia reperfusion injury and improve the neurological function of rats.
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Objective To investigate the regulating effects and mechanism of Laminaria japonica (L.japonica) on serum lipid of hyperlipidemia rats.Methods Forty healthy female Wistar rats were used to establish hyperlipidemia models by feeding fat-rich forage,and the powder of L.japonica was applied as a supplement in forage for test groups.The levels of serum lipid including the triglyceride(TG),total cholesterol(TC),low-density lipoprotein (LDL),high-density lipoprotein(HDL) and the activities of lipoproteinesterase(LPL) and hepatic lipase(HL) were detected by biochemical assay.Results The levels of serum TG and TC in test group decreased significantly than those in pre-treated and model group (P
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Aim To study the interfering effects of picroside Ⅱ on the expressions of nuclear transcription factor kappaB(NF-?B)and inhibitor of NF-?B(I-?B) after cerebral ischemic reperfusion in rats. Methods Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion models in rats. PicrosideⅡ(10 mg?kg-1) and salvianic acid A sodium(10 mg?kg-1 ) were injected from the tail vein for treatment. TUNEL positive cells were counted by immunofluorescence assay. The expressions of NF-?B and I-?B were determined by immunohistochemical assay,and the concentration of NF-?B and I-?B in brain tissue was determined by ELISA. Results The exprssions of NF-?B and I-?B were weakly and the apoptotic cells were scattering at cortex,striatum and hip-pocampus in the sham operative group. In the negative control group,the number of TUNEL positive cells and the expressions of NF-?B and I-?B increased,the absorption(A) values and the concentration were significantly higher than those in the sham operative group(P0.05 ). Conclusion Picroside Ⅱ might downregulate the expressions of NF-?B and I-?B to inhibit neuronal apoptosis induced by inflammation after cerebral ischemia reperfusion injury in rats.