Effect of ilexonin A on proliferation and migration of bone mesenchymal stem cells in rats / 中国药理学通报

Aim To observe the effect of ilexonin A (IA) on the proliferation of bone marrow mesenchymal stem cells(BMSCs),and to investigate whether IA can promote the migration of BMSCs by up-regulating the expression of CXCR4 in rats. Methods MTT method was used to assay and analyse the proliferation of BM-SCs which were pretreated with different concentrations of IA (3.125,6.25,12.5,25,50,100,200,400, 800 mg·L-1) for 24,48 and 72h,then the best con-centration and the best optimum time were screened. The third generation of BMSCs was exposed to the opti-mal concentration of IA for 48h. The Transwell system was used to carry out the experiment of BMSCs migra-tion. Western blot was used to analyse the expression of CXCR4. Results MTT assay showed that com-pared with control group, the proliferation of BMSCs was significantly reduced in IA 100 ~800 mg·L-1 groups at 24h(P < 0.05); compared with control group, the proliferation of BMSCs significantly de-creased in IA 100~800 mg·L-1groups at 48h(P<0.05),but markedly increased in IA 6.25 and 3.125 mg·L-1groups (P <0.05); compared with control group,the proliferation of BMSCs was significantly re-duced in IA 12.5~800 mg·L-1groups at 72h(P<0.05). The above results indicated that the BMSCs in-cubated with IA 6.25 and 3.125 mg·L-1for 48h were the optimal choice to promote proliferation. The Transwell migration assay showed that incubation with IA 6.25 and 3.125 mg·L-1for 48h could significant-ly increase the migration of BMSCs(P <0.05), and the migration rate was not related with the concentra-tion of IA. This effect was completely blocked by AMD3100(the antagonist of CXCR4). Western blot showed that incubation with IA 6.25 and 3.125 mg· L-1for 48h could increase the expression of CXCR4 in BMSCs(P<0.05). Conclusion IA can promote the proliferation of BMSCs and increase the migration of BMSCs by up-regulating the expression of CXCR4.

Changes of left ventricular remodeling in hypertension patients with carotid atherosclerosis of phlegm-dampness syndrome / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study changes of left ventricular remodeling (LVR) in hypertension patients with carotid atherosclerosis (CAS) of phlegm-dampness syndrome (PDS).</p><p><b>METHODS</b>Doppler ultrasonography data of CAS were observed in 223 hypertension patients with CAS (as the hypertension group, including 119 patients of the PDS group and 104 of the non-PDS group), 81 CAS patients with non-hypertension, and 19 non-hypertension non-CAS patients (as the control group). The difference in the degree of LVR was compared among the above groups.</p><p><b>RESULTS</b>The left ventricular posterior wall thickness (LVPWT), inter ventricular septum thickness (IVS), E/A were higher in the hypertension group than in the non-hypertension group (P < 0.05). The left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic diameter (LVESD), stroke volume (SV) were higher in the soft plaque hypertension group and the soft plaque non-hypertension group than in the hard plaque group, the thickening intimal group, and the normal intimal group (P < 0.01 , P < 0.05). The LVEDD, LVESD, and SV were higher, and the ejection fraction (EF) was lower in the PDS hypertension group than in the non-PDS hypertension group (all P < 0.05). Of them, LVEDD, LVESD, and SV were higher in the soft plaque group than in the hard plaque group (P < 0.01), the thickening intimal group (P < 0.01) and the normal intimal group (P < 0.05). There was no statistical difference in PDS hypertension between the soft plaque group and the hard plaque group (P > 0.05).</p><p><b>CONCLUSION</b>The hypertension patients with CAS of PDS might be correlated to LVR, and LVR was more obviously in the soft plaque patients.</p>

The expression of bFGF, GAP-43 and neurogenesis after cerebral ischemia/reperfusion in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To observe time points of the expressions of basic fibroblast growth factor (bFGF), growth associated protein-43 (GAP-43) and neurogenesis after cerebral ischemia/reperfusion in rats and explore its possible mechanism of neurogenesis.</p><p><b>METHODS</b>Models of middle cerebral artery occlusion (MCAO) were established in SD rats which were divided into 3 d, 7 d, 14 d and 28 d groups (n = 6). The neurological severity was evaluated by neurological severity scores (NSS) and scores of motor test (SMT). Neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Nissl staining; The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blot and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively.</p><p><b>RESULTS</b>It showed up neurologic impairment and motor dysfunction after cerebral ischemia/reperfusion in rats at 3 d, the numbers of neuron apoptosis also peaked at 3d, the protein levels of bFGF and GAP-43 were significantly increased in time-dependent manner, peaked at 7 d and then decreased gradually, meanwhile, Brdu and NeuN double fluorescence staining displayed scattered Brdu-and NeuN-positive cells in the boundary zone of the infarction area.</p><p><b>CONCLUSION</b>These results suggest that the upregulation of bFGF and GAP-43 may contribute to the neurogenesis after cerebral ischemia/reperfusion.</p>

Mechanism of the reduction of cerebral ischemic-reperfusion injury through inhibiting the activity of NF-kappaB by propyl gallate / 药学学报

The probable mechanism of the reduction of rat cerebral ischemic-reperfusion injury by propyl gallate was studied. Intraluminal suture middle cerebral artery occlusion model of rat was employed. Propyl gallate was injected immediately after the ischemia was happened. The activity of NF-kappaB, and the expression of COX-2 and HSP70 on the peripheral ischemia were determined by Western blotting. The expression of TNF-alpha was determined by ELISA assay. RT-PCR and immunofluorescence staining were employed to detect the transcription and expression of TLR-4. Results showed that propyl gallate could inhibit the activity of NF-kappaB in the peripheral ischemia, and reduce the expression of COX-2 and TNF-alpha. As the upstream of NF-kappaB, the transcription and expression of TLR-4 decreased, as well as HSP70, the endogenic ligand of TLR-4. As an antioxidant, propyl gallate could reduce the cerebral ischemic-reperfusion injury through inhibiting the activity of NF-kappaB and decreasing the COX-2 and TNF-alpha in the peripheral ischemia. It also could influence HSP70 and TLR-4.

Correlation study between carotid atherosclerosis and hypertension / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the correlation between carotid atherosclerosis (CAS) and hypertension.</p><p><b>METHODS</b>Color Doppler ultrasonography data of CAS were observed in 150 hypertension patients [as the hypertension group, including 70 patients in the phlegm-stasis syndrome (PSS) group and 80 in the non-PSS group] and 30 non-hypertension patients (as the control group). The difference of the CAS occurrence was compared among the three groups.</p><p><b>RESULTS</b>The incidence of CAS was higher in the PSS group and the non-PSS group than in the control group, showing statistical difference (P<0.01). Of them, it was higher in the PSS group than in the non-PSS group (P<0.05). Hard plaque dominated in the CAS plaque constitution in both the PSS group and the non-PSS group. Of them the soft plaque ratio was higher in the PSS group than in the non-PSS group, showing statistical difference (41.9% vs 11.4%, P<0.05). The CAS plaque distribution positions among the three groups (P>0.05). The inner diameters of the left and right common carotid artery, and the resistant indices of the left and right common carotid artery, the left internal carotid artery, and the left vertebral artery in the PSS group and the non-PSS group were higher than in the control group (P<0.05).</p><p><b>CONCLUSIONS</b>Hypertension patients are often accompanied with CAS of various degrees. Especially the soft plaque ratio of the CAS plaque was higher in those of PSS, indicating the possibility of target organs damage such as cerebral infarction was higher.</p>

Influence of ilexonin A on the expression of bFGF, GAP-43 and neurogenesis after cerebral ischemia-reperfusion in rats / 药学学报

This study is to observe the effect of ilexonin A (IA) on the expression of basic fibroblast growth factor (bFGF) and growth associated protein-43 (GAP-43), and neurogenesis after cerebral ischemia-reperfusion in rats and explore its possible mechanism of protecting neuronal injury. Models of middle cerebral artery occlusion (MCAO) were established in SD rats. Before and after two hours ischemia-reperfusion, IA (20 and 40 mg x kg(-1)) was injected immediately and on 3, 7, 14, and 28 d once a day. The neurological severity was evaluated by neurological severity scores (NSS); neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Niss1 staining. The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blotting and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. After treatment with IA, the NSS of treatment groups were lower than that of the models (3 and 7 d). The number of TUNEL positive neurons decreased and Nissl positive neurons increased at the same time (3 d). The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. Moreover, IA markedly enhanced the neurogenesis in the brain after ischemia-reperfusion, which revealed an increase of Brdu/NeuN positive cells in the boundary zone of the infarction area. The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion.

Relationship between carotid atherosclerosis and cerebral infarction / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To study the relationship between carotid atherosclerosis and cerebral infarction (CI).</p><p><b>METHODS</b>Between November 2008 and March 2009, 147 CI patients (CI group) and 48 patients with non-cerebrovascular diseases (control group) were enrolled from inpatients of Neurology Department of our hospital. The diagnostic criterion of thickened carotid intima was set as 1.0 mm<intima-media thickness (IMT) < 1.5 mm and that of carotid plaque was as IMT 1.5 mm. Carotid atherosclerosis was divided into three levels: normal intima, thickened intima, and plaque formation. The color Doppler ultrasonography data of carotid arteries in all patients were analyzed and the severity of carotid atherosclerosis was compared between the two groups.</p><p><b>RESULTS</b>In the CI group, 36 (24.5%) patients had normal carotid intima, 22 (15.0%) had thickened carotid intima, and 89 (60.5%) had carotid plaque. In the control group, 22 (45.8%) patients had normal carotid intima, 4 (8.3%) had thickened carotid intima, and 22 (45.8%) had carotid plaque. The severity of carotid atherosclerosis in the CI group was higher than that in the control group (P = 0.022). There was significant difference in the constitution of carotid plaque between the two groups (P = 0.001); the CI group mainly had the soft plaque (55/89, 61.8%), whereas the control group mainly had the hard plaque (17/22, 77.3%). The first three common locations of carotid plaque in both groups were carotid bifurcation (CI group: 73.7%; control group: 64.1%), common carotid artery (CI group: 20.4%; control group: 25.6%), and internal carotid artery (CI group: 5.9%; control group: 10.3%). The location of carotid plaque between the two groups was not significantly different (P = 0.438). There was no difference in the carotid inner diameter or resistance index between the two groups (P > 0.05).</p><p><b>CONCLUSIONS</b>Carotid atherosclerosis is to some extent able to reveal the atherosclerotic condition of cerebral arteries and act as an important predictor for the risk of CI. The color Doppler ultrasonography of carotid arteries can provide a convenient way for the prevention and treatment of CI.</p>

Inhibitory action of propyl gallate on the activation of SAPK/JNK and p38MAPK induced by cerebral ischemia-reperfusion in rats / 药学学报

<p><b>AIM</b>To explore the protective effect of propyl gallate against neuronal injury in the boundary zone of the infarction area in the rat cerebral ischemia-reperfusion model and its possible mechanism.</p><p><b>METHODS</b>Transient focal ischemia induced by middle cerebral artery occlusion in the rats was established by ligation of the left internal carotid artery for 2 h. Rats were treated by propyl gallate with different doses (23.5, 47 and 94 micromol x kg(-1)) for three days before operation. Coronal brain sections were collected after 1 , 2, 4, 6, 12 and 24 h of reperfusion, neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Nissl staining. The expression of activated Caspase-3, total SAPK/JNK, p38MAPK and their phosphorylation (Thr183/Tyr185, Thr180/Tyr182) was investigated by immunohistochemistry and Western blotting with corresponding antibodies.</p><p><b>RESULTS</b>Although SAPK/JNK immunoreactivity did not increase at each time point in the boundary zone of the infarction area after reperfusion, p-SAPK/JNK immunoreactivity increased significantly at 1 h and then decreased gradually, and p38MAPK immunoreactivity was enhanced at each time point, peaked at 6 h. Expression of p-p38MAPK peaked at 6 h. Activated Caspase-3 immunoreactivity appeared at 6 h in the boundary zone of the infarction area and peaked at 12 h. TUNEL positive neurons were observed at 12 h and became more abundant at 24 h. The number of Nissl positive neurons decreased gradually and apoptosis ratio of neurons peaked at 24 h. Propyl gallate reduced the immunoreactivity of SAPK/JNK, p-SAPK/JNK, p38MAPK and p-p38MAPK markedly at 1 and 6 h. Propyl gallate with doses of 47 and 94 micromol x kg(-1) were more effective.</p><p><b>CONCLUSION</b>Inhibition on the activation of SAPK/JNK and p38MAPK is the possible protective mechanism of propyl gallate against neuronal injury induced by cerebral ischemia-reperfusion.</p>