Shen-Zhi-Ling oral solution improves learning and memory ability in Alzheimer's disease mouse model.

OBJECTIVE: To investigate the effector mechanisms and effector targets of Shen-Zhi-Ling (SZL) oral solution in the treatment of Alzheimer's disease (AD). METHODS: In this study, we carried out gavage with SZL oral solution in an APP/PS-1 heterozygous double transgenic AD mouse model for 12 continuous weeks. Haematoxylin and eosin staining, Nissl staining and Annexin V/Propidium Iodide staining were used to detect the brain histopathology in AD mouse model. Immunofluorescence staining was used to detect the expression levels of autophagy's proteins. Morris water maze test was used to detect the learning and memory ability in AD mouse model. RESULTS: Pathological results showed that neuronal loss in the hippocampus of mice in the SZL intervention group was significantly alleviated and the number of apoptotic neurons was significantly decreased compared with the control group (physiological saline and non-intervention groups). Immunofluorescence staining results showed that the expression of autophagy activators, Beclin-1 and LC3B, was significantly increased in the hippocampal neurons of mice of the SZL intervention group, while the expression of the apoptotic factor, caspase-3, was significantly decreased. At the same time, hippocampal accumulation of Aß42 protein was significantly decreased. In addition, results of the water maze experiment showed that the latency period in mice from the SZL intervention group was significantly reduced. CONCLUSION: In summary, we believe that the SZL oral solution significantly activates autophagy in hippocampal neurons, effectively reducing the accumulation of Aß42 peptides, alleviating neuronal injury and apoptosis, and ultimately improving the cognitive function in a mouse model of AD.

Synergistic anti-hepatoma effect of bufalin combined with sorafenib via mediating the tumor vascular microenvironment by targeting mTOR/VEGF signaling.

Sorafenib inhibits tumor growth primarily by inhibiting vessel formation, however, its efficacy requires improvement, therefore, the development of strategies which augment its antiangiogenic effect are of primary concern. Bufalin inhibits tumor cell proliferation and metastasis, and induces apoptosis. In our previous study, it was demonstrated that the antiangiogenic effect of sorafenib was improved by bufalin in human umbilical vein endothelial cells (HUVECs). However, whether bufalin synergizes with sorafenib by affecting the tumor vascular microenvironment remains to be elucidated. In the present study, it was found that hepatocellular carcinoma (HCC) cell proliferation was inhibited by either bufalin or sorafenib following incubation for 24 h, and the inhibition was enhanced upon treatment with a combination of the two. Conditioned medium (CM), comprising supernatant from HCC cells was collected from each of the treatment groups. The migration and tubule formation were suppressed the most in the combination-CM treated HUVECs. The secretion of vascular endothelial growth factor (VEGF) was decreased in HCC cells treated with the combination-CM, as determined by an angiogenesis array, enzyme-linked immunosorbent assay (ELISA) and western blot analysis. The inhibition of tube formation in HUVECs treated with the combination-CM was reversed by incubation with VEGF. The in vivo experiments demonstrated that subcutaneous HCC cell tumors from mice treated with the combination treatment expressed the lowest levels of VEGF, as evidenced by immunohistochemistry and ELISA. Additionally, the level of phosphorylated mechanistic target of rapamycin (mTOR) was reduced in HUVECs pretreated with the phosphoinositide 3-kinase inhibitor PI103. Furthermore, the migration of HCC cells and HUVEC tube formation were attenuated by PI103 pretreatment. In conclusion, the results revealed a synergistic anti-hepatoma effect of bufalin combined with sorafenib via affecting the tumor vascular microenvironment by targeting mTOR/VEGF signaling.

Synergistic anticancer effects of bufalin and sorafenib by regulating apoptosis associated proteins.

As one of the most recognized and well­known drugs for hepatocellular carcinoma (HCC), the antitumor effect of sorafenib against HCC remains to be improved. Bufalin has displayed an antitumor effect in HCC; however, whether the enhanced antitumor effect may be generated with their combined treatment remains unclear. Therefore, in the present study, their combined effects on HCC proliferation and apoptosis were investigated. It was revealed that either bufalin or sorafenib suppressed PLC/PRF/5 and SMMC­7721 cell proliferation in a concentration­dependent manner following incubation for 24 h, and the inhibitory effect was augmented with their combined treatment. The synergistic effect peaked in HCC cells treated with 20 nM bufalin and 10 µM sorafenib. In addition, cell cycle and terminal deoxynucleotidyl transferase dUTP nick­end labelling assays revealed that bufalin also enhanced sorafenib­induced apoptosis. Colony formation assay demonstrated that combined treatment significantly suppressed HCC proliferation compared with treatment with either of them alone. Furthermore, B­cell lymphoma 2­associated X protein, caspase 7 and poly­(adenosine diphosphate­ribose) polymerase were upregulated in HCC cells with combined treatment. Taken together, the results of the present study revealed that the treatment of sorafenib combined with bufalin synergistically suppressed HCC proliferation and induced apoptosis. Therefore, bufalin combined with sorafenib may be a favorable treatment strategy for patients with HCC.

How many ELNs are optimal for breast cancer patients with more than three PLNs who underwent MRM? A large population-based study.

BACKGROUND: Few studies have focused on the optimal threshold of examed lymph nodes (ELNs) for breast cancer patients with more than three positive lymph nodes after modified radical mastectomy. MATERIALS AND METHODS: The X-tile and the minimum P-value models were applied to determine the optimal threshold. Cox proportional hazard analysis was used to analyze the cancer-specific survival and perform subgroup analysis. RESULTS: The results showed that 12 ELNs was the optimal threshold for these patients, and the patients with >12 ELNs had a better cancer-specific survival benefit compared with the patients with <12 ELNs (P<0.001). CONCLUSION: The number 12 can be selected as the optimal threshold of ELNs for breast cancer patients with >3 positive lymph nodes after modified radical mastectomy.

Salidroside slows the progression of EA.hy926 cell senescence by regulating the cell cycle in an atherosclerosis model.

Aging is the major risk factor for diseases of the cardiovascular system, such as coronary atherosclerotic heart disease, but little is known about the relationship between atherosclerosis (AS) and age­related declines in vascular structure and function. Here, we used histological analyses in combination with molecular biology techniques to show that lipid deposition in endothelial cell was accompanied by aging and growth arrest. Endothelial cell senescence is sufficient to cause AS; however, we found that salidroside reduced intracellular lipid deposition, slowed the progression of endothelial cell senescence and inhibited the expression of the senescence­related molecules and phosphorylated the retinoblastoma (Rb) protein. Further study confirmed that salidroside increased the percent of S phase cells in oxidized low­density lipoprotein (ox­LDL)­treated endothelial cells. Collectively, vascular endothelial cell function declined with age and AS, and our data suggested that salidroside prevented ox­LDL­treated endothelial cell senescence by promoting cell cycle progression from G0/G1 phase to S phase via Rb phosphorylation. We demonstrated for the first time the complex interactions between AS and endothelial cell senescence, and we believe that salidroside represents a promising therapy for senescence­related AS.

Effect of the herbal formulation Shen-Zhi-Ling on an APP/PS1 mouse model of Alzheimer's disease by modulating the biliverdin reductase/heme oxygenase 1 system.

Shen-Zhi-Ling (SZL) oral liquid is a traditional Chinese medicine formula that is mainly used for the clinical treatment of mild to moderate Alzheimer's disease (AD). The aim of the present study was to investigate the effects and underlying mechanisms of SZL treatment on AD. APP/PS1 transgenic mice were utilized to evaluate the effect of SZL treatment (0.5 g/20 g/day). Morris water maze and Thioflavin S staining analyses were used to evaluate the cognitive impairment and ß-amyloid plaques, respectively, while quantitative polymerase chain reaction and western blot analysis were performed to examine the mRNA and protein expression levels of heme oxygenase 1 (HO-1) and biliverdin reductase (BVR). Furthermore, immunofluorescence staining was used to measure the BVR and HO-1 protein levels in the hippocampus. The findings of the current study demonstrated that SZL treatment was able to ameliorate the impairment of memory and reduce the accumulation of amyloid plaques, and its ameliorating effects may be attributed to the modulation of the HO-1/BVR system in the hippocampus. These results indicate that SZL may be a possible complementary and alternative therapy to delay the development of AD.

The appropriate number of ELNs for lymph node negative breast cancer patients underwent MRM: a population-based study.

Whether number of examed lymph nodes (ELNs) would bring survival benefit for patients with negative lymph nodes after modified radical mastectomy (MRM) is uncertain. In our study, using the Surveillance Epidemiology and End Results (SEER) database between 2004 and 2009, we screened the appropriate patients with negative lymph nodes underwent MRM. The Cox proportional hazard analysis was used to determine the effect of number of ELNs on cancer specific survival (CSS). The results showed that the number of ELNs was not an independent prognostic factor on CSS (P = 0.940). Then the X-tile mode was used to determine the appropriate threshold for ELNs count. The results showed that 9 was the appropriate cut-off point. Next, the log-rank χ2 test was used to analyze the CSS based on different subgroup variables. The results showed that some subgroup variables including age < 50/ ≥ 50, grade I/III, AJCC T1/T2, ER positive/negative and PR positive/negative ,demonstrated significant CSS benefits among the patients with the number of ELNs ≤ 9 (all, P < 0.05). However, three subgroup variables including grade II, AJCC T3 and AJCC T4, the patients with the number of ELNs ≤ 9 did not bring significant CSS benefits (all, P > 0.1). In conclusion, our study demonstrated that the number of ELNs was not an independent prognostic factor on CSS, and 9 can be selected as the appropriate cut-off point of ELNs for patients with negative lymph nodes who underwent MRM.

Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR.

Many studies have demonstrated that curcumin can effectively inhibit the proliferation, invasion, and tumorigenesis of prostate cancer cells in vitro and in vivo. In this study, CD44+/CD133+ human prostate cancer stem cells (HuPCaSCs) were isolated from the prostate cancer cell lines Du145 and 22RV1. Curcumin treatment of these cells resulted in the inhibition of in vitro proliferation and invasion, and cell cycle arrest. The expression levels of cell cycle proteins (Ccnd1 and Cdk4) and stem cell markers (Oct4, CD44, and CD133) were decreased in curcumin-treated HuPCaSCs. Microarray analysis and northern blotting assays indicated that miR-145 was overexpressed in curcumin-treated HuPCaSCs. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were gained from bioinformatic analysis, bioinformatics analysis and luciferase activity assays showed that the lncRNA-ROR and Oct4 mRNA both contain miR-145 binding sites, and Oct4 and lncRNA-ROR directly compete for microRNA binding. Curcumin induced high miR-145 expression and inhibited the expression of lncRNA-ROR. The tumorigenicity of curcumin- treated HuPCaSCs in nude mice was significantly reduced. In summary, reducing the expression of endogenous lncRNA-ROR could effectively increase the available concentration of miR-145 in HuPCaSCs, where miR-145 prevents cell proliferation by decreasing Oct4 expression. In particular, we hypothesized that lncRNA-ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Oct4. Thus, curcumin suppresses the proliferation, in vitro invasion, and tumorigenicity of HuPCaSCs through ceRNA effect of miR-145 and lncRNA-ROR caused.

Cyclophosphamide promotes the proliferation inhibition of mouse ovarian granulosa cells and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.

The dysfunction of ovarian granulosa cells (OGCs) directly affects the premature ovarian failure (POF). In vivo experiments showed that cyclophosphamide significantly induced mouse ovarian atrophy and proliferation inhibition of OGCs. The expressions of p53, p66Shc and p16 were significantly higher in OGCs of the cyclophosphamide treatment group. MTT assay showed that cyclophosphamide effectively inhibited the proliferation of OGCs in vitro. SA-ß-Gal staining showed that the OGCs in the cyclophosphamide treatment group had many senescent cells. And, the expression of p53, p66Shc, p16 and cleaved caspase-3 in the OGCs of the cyclophosphamide treatment group significant increases. The Northern blot showed that the intensity of the lncRNA-Meg3 hybridization signal of the OGCs in the cyclophosphamide treatment group was significantly higher than that in the control group. ChIP results confirmed the significant increase in the obtained p66Shc promoter DNA fragment, which was enriched on p53 protein, in the OGCs treated with cyclophosphamide. When cyclophosphamide treatment was conducted after siRNA-Meg3 was used, the expression of endogenous lncRNA-Meg3, p53, p66Shc, p16 and cleaved caspase-3 was significantly lower than that in the siRNA-Mock control group. In summary, cyclophosphamide promotes the proliferation inhibition of mouse OGCs and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.

Bufalin suppresses hepatocellular carcinoma invasion and metastasis by targeting HIF-1α via the PI3K/AKT/mTOR pathway.

It has been reported that there are multiple mechanisms by which bufalin could exert its antimetastatic effect. HIF-1α has been reported to be involved in tumor migration and invasion by regulating EMT. However, it is not known whether bufalin could exert the antimetastatic effect by modulating HIF-1α expression in hepatocellular carcinoma. In the present study, we aimed to evaluate the antimetastatic potential of bufalin in vivo and in vitro. Our results demonstrated that the liver/lung metastases were significantly reduced in bufalin-treated mice, as tested in the orthotopic transplanted and tail vein injection tumor models. Furthermore, the epithelial-to-mesenchymal transition (EMT) was inhibited in bufalin-treated tumors, as reflected the upregulation of E-cadherin, and downregulation of N-cadherin, vimentin, Snail. Similar results were observed in SMMC7721 cells treated with bufalin. Moreover, the transforming growth factor-ß1 (TGF-ß1)-induced EMT was also abrogated by bufalin. Mechanistically, our study demonstrated that hypoxia-inducible factor-1α (HIF-1α) played an important role in the antimetastatic effect of bufalin in hepatocellular carcinoma. Importantly, HIF-1α expression may be regulated through the inhibition of the PI3K/AKT/mTOR pathway. Taken together, our results suggest that bufalin suppresses hepatic tumor invasion and metastasis and that this process may be related to the PI3K/AKT/mTOR/ HIF-1α axis.

Small molecule compounds alleviate anisomycin-induced oxidative stress injury in SH-SY5Y cells via downregulation of p66shc and Aß1-42 expression.

Oxidative stress and ageing are important factors contributing to the pathogenesis of Alzheimer's disease (AD), which is associated with neuronal damage and ß-amyloid (Aß) deposition. The p66shc adaptor protein is important for the regulation of oxidative stress and ageing. In the present study, SH-SY5Y human neuroblastoma cells were treated with anisomycin in order to establish a cell model of oxidative stress-induced neuronal damage. The results from quantitative polymerase chain reaction, enzyme-linked immunosorbent assay and western blotting demonstrated that anisomycin was able to stimulate the secretion of Aß1-42 from SH-SY5Y cells and upregulate the expression levels of p66shc, which was associated with concomitant damage to SH-SY5Y cells. In addition, the protective effects of various small molecule compounds with antioxidant properties against neuronal damage were evaluated. Notably, treatment of SH-SY5Y cells with gallic acid was associated with significant downregulation of p66shc protein expression levels, reduced anisomycin-induced secretion of Aß1-42, and increased superoxide dismutase activity and acetylcholine secretion levels. The results of the present study suggested that anisomycin is able to promote oxidative neuronal damage by inducing the secretion of Aß1-42 from neurons and increasing the neuronal expression of p66shc, and this damage may be attenuated by treatment with gallic acid. Therefore, gallic acid and similar small molecule compounds may be considered for the alleviation of neuronal oxidative stress injury in patients with AD.

Activation of phosphatidylinositol 3-kinase/Akt signaling mediates sorafenib-induced invasion and metastasis in hepatocellular carcinoma.

Sorafenib, an antiangiogenic agent, can promote tumor invasion and metastasis. The phosphatidylinositol 3-kinase (PI3K)/Akt/Snail-dependent pathway plays an important role in tumor invasion and metastasis. Yet, little is known concerning the role of the PI3K/Akt/Snail-dependent pathway in sorafenib­induced invasion and metastasis of hepatic carcinoma (HCC). A human HCC orthotopic xenograft model was established, and sorafenib (30 mg/kg/day) was administered orally. Tumor growth and intrahepatic metastasis were assessed, and immunohistochemistry was applied to analyze the activation of the PI3K/Akt/Snail-dependent pathway. HCC cell lines were treated with sorafenib (1, 5 and 10 µM), and proliferation, migration and invasion were assessed. Western blotting and real-time polymerase chain reaction (RT-PCR) were used to examine the related gene expression of epithelial-mesenchymal transition (EMT) markers and the PI3K/Akt/Snail-dependent pathway. Sorafenib inhibited tumor growth and promoted intrahepatic invasion and metastasis of the orthotopic tumors grown from SMMC7721-GFP cells in vivo. Additionally, sorafenib promoted EMT and invasion and metastasis of HCC cells in vitro. Importantly, sorafenib enhanced PI3K and Akt activation and upregulation of the expression of transcription factor Snail, a critical EMT mediator. The upregulation of transcription factor Snail expression by sorafenib may be related to activation of the PI3K/AKT signaling pathway. The PI3K/Akt/Snail-dependent pathway may mediate the pro-invasive and pro-metastatic effects of sorafenib on HCC by inducing EMT.

Attenuated ability of BACE1 to cleave the amyloid precursor protein via silencing long noncoding RNA BACE1­AS expression.

Although large numbers of long noncoding RNAs (lncRNAs) expressed in the mammalian nervous system have been detected, their functions and mechanisms of regulation remain to be fully clarified. It has been reported that the lncRNA antisense transcript for ß­secretase­1 (BACE1­AS) is elevated in Alzheimer's disease (AD) and drives the rapid feed­forward regulation of ß­secretase, suggesting that it is critical in AD development. In the present study, the senile plaque (SP) AD SH­SY5Y cell model was established using the synthetic amyloid ß­protein (Aß) 1­42 in vitro. Using this model, the potential of siRNA­mediated silencing of lncRNA BACE1­AS expression to attenuate the ability of ß­secretase­1 (BACE1) to cleave amyloid precursor protein (APP) and to reduce the production of Aß1­42 oligomers was investigated. MTT assays demonstrated that exogenous Aß1­42 suppressed SH­SY5Y cell proliferation and induced APP­related factor expression and SP formation. Furthermore, quantitative polymerase chain reaction and western blot analysis revealed that the mRNA and protein expression of Aß1­42 and Aß1­40 was significantly increased in the AD model group, with a marked decrease in Ki­67 expression at day six. RNase protection assays (RPA) and northern blotting analysis confirmed that exogenous Aß1­42 not only promoted the expression of the APP­cleaving enzyme BACE1, but also induced lncRNA BACE1­AS expression. Furthermore, lncRNA BACE1­AS formed RNA duplexes and increased the stability of BACE1 mRNA. Downregulation of lncRNA BACE1­AS expression in SH­SY5Y cells by siRNA silencing resulted in the attenuation of the ability of BACE1 to cleave APP and delayed the induction of SP formation in the SP AD SH­SY5Y cell model.

Transplantation of human menstrual blood stem cells to treat premature ovarian failure in mouse model.

The incidence of premature ovarian failure (POF), also known as ovarian insufficiency, has been increasing in recent years. Although some treatments are currently available, improved treatment strategies are urgently required. Many researchers have reported that human endometrial stem cells (HuMenSCs), which exhibit stem/progenitor cell properties in vitro repaired damaged cells in vivo. Thus, we aimed to determine whether HuMenSCs can serve as cell therapy tools and be used for the treatment of POF. After treating with cyclophosphamide, on the first estrus period (we predicted mouse estrus cycle was generally 5 days), HuMenSCs were injected into a cyclophosphamide-induced mouse model of POF. The results revealed that the HuMenSCs could survive within POF mouse ovaries for at least 14 days in vivo; further, ovaries of the HuMenSCs-transplanted group expressed higher levels of ovarian markers [AMH, inhibin α/ß, and follicle-stimulating hormone receptor (FSHR)], and the proliferative marker Ki67. In addition, the ovarian weight, plasma E2 level, and the number of normal follicles increased over time in the HuMenSC group compared with the control group. Further, microarray analysis of cDNA expression patterns revealed that, after HuMenSC transplantation, the gene mRNA expression patterns in the ovarian cells following stimulation of the host ovarian niche became increasingly similar to those observed in human ovarian tissue compared with the pretransplantation mRNA expression pattern in HuMenSCs. Hence, we can safely conclude that the mesenchymal stem cell properties and in vivo survival of HuMenSCs make them ideal seed cells for stem cell transplantation in the treatment of POF.

Attenuation of exogenous angiotensin II stress-induced damage and apoptosis in human vascular endothelial cells via microRNA-155 expression.

Numerous studies have indicated that cells and tissues have means of blocking their response to continuous stress signals to protect themselves from damage. Overexpression of angiotensin II (Ang II) in the renin-angiotensin system can cause vascular endothelial damage, but the mechanism of adjustment of the dynamic equilibrium remains unclear. In this study, we investigated whether microRNA-155 (miR-155) can suppress continuous Ang II stress signals that would otherwise cause vascular endothelial damage. We isolated and cultured human umbilical vein endothelial cells (HUVECs) and transfected one group of these with a mature miR-155 expression plasmid. Quantitative real-time PCR (qRT-PCR) and western blotting showed Ang II type 1 receptor expression to be decreased in miR-155-transfected HUVECs compared with untransfected cells. The MTT proliferation assay revealed that exogenous Ang II suppressed proliferation of HUVECs in a concentration-dependent manner. When HUVECs were cultured in medium containing Ang II at the half maximal inhibitory concentration (68.94 ng/µl) for 24 h, qRT-PCR and western blotting showed that expression of the apoptosis inhibitor Bcl-2 in the HUVEC-Ang II group was markedly lower than that in controls, but apoptosis-promoting factors (Bax, cytochrome c, caspases-9 and -3) were not. Co-immunoprecipitation western blotting and immunofluorescence staining showed that exogenous Ang II increased the phosphorylation and activation of extracellular signal related kinase (ERK)1/2. Exogenous Ang II also influenced HUVEC migration and capillary tubule formation in vitro. However, after transfection of HUVECs with miR-155 under the same conditions, expression of apoptosis-promoting factors and ERK1/2 phosphorylation were reduced significantly and HUVEC migration and capillary tubule formation were restored to some extent. Thus, miR-155 attenuated the effect of exogenous Ang II-induced ERK1/2 activation to reduce HUVEC damage and apoptosis. Moreover, miR-155 maintained HUVEC migration and capillary tubule formation in vitro.

[Effects of Chinese herbal medicine Shoushen Granule on telomere length and telomerase activity of peripheral white blood cells and vascular cells in rats with atherosclerosis].

OBJECTIVE: To observe the effects of Shoushen Granule, a compound traditional Chinese herbal medicine, on telomere length and telomerase activity in peripheral leukocytes and vascular cells, artery wall lesions and blood lipid in a Sprague-Dawley (SD) rat model of atherosclerosis. METHODS: Forty SD rats were randomly divided into normal control group, model group, Shoushen Granule group and Western medicine group with 10 in each group. The rat model of atherosclerosis was established by high-fat diet and vitamin D3 loading. The model group was given gastric perfusion of double distilled water; The Shoushen Granule group and the Western medicine group were respectively given gastric perfusion of Shoushen Granule and pravastatin. After 12 weeks, pathological changes of abdominal aorta were determined by hematoxylin and eosin staining. Biochemical colorimetric method was used to detect the contents of total cholesterol (TC), triacylglycerol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol (LDL-C) in serum of the rats. Telomere length and telomerase activity in peripheral leukocytes and vascular cells of the rats were tested by quantitative real-time polymerase chain reaction method. RESULTS: When compared with the model group, atherosclerosis lesions of the arterial wall were significantly improved in the Shoushen Granule group. In addition, both TC and LDL-C levels in the Shoushen Granule group were decreased significantly compared with the model group (P<0.01). Besides, not only telomerase activity but also telomere length in peripheral leukocytes (P<0.01) and vascular cells (P<0.05) were increased significantly as compared to those in the model group. However, there was no significant difference between the Shoushen Granule group and the normal control group (P>0.05). CONCLUSION: Shoushen Granule improves the atherosclerosis lesions in rats, and the mechanism may be related to regulating telomere length and telomerase activity.

[To investigate the strategy of Chinese medicine for prevention and treatment of atherosclerosis based on vascular aging].

Atherosclerosis, a chronic degenerative disease mainly attacks the middle-aged and the aged population as they grow old. Anti-angiocellular aging has gradually become a new strategy for atherosclerosis. In the process of atherosclerosis developing, endothelial cell renewing is speeding. Various biological function disorders that induce blood vessel aging emerge, which leads to changes of the telomere and telomerase, resulting in aged endothelial cells and dysfunction. Telomere and telomerase may play key roles in the etiological factors such as inflammation and AS plaque. In our previous work we have found that Chinese compounds with Shen invigorating effects could not only obviously ameliorate the symptoms and functions of the senility, but also show significant effects on restraining atherosclerosis. We should actively study the mechanisms of Chinese medicine for treating atherosclerosis from Shen, and the mechanisms of Shen invigorating compounds for regulating angiocellular aging through the telomere pathway, thus providing evidence for establishing vascular cell aging based atherosclerosis prevention and treatment strategies by Chinese medicine.