Influence of the gastrointestinal microflora and efflux transporters on the absorption of scutellarin and scutellarein.

Scutellarin (SG) and its aglycone, Scutellarein (S), are flavonoids of therapeutic cardiocerebrovascular disease. SG was hydrolyzed by bacterial enzyme into S which was absorbed in the intestine. The aim of this study was to determine the effects of the microflora in the intestinal lumen and the efflux transporter of intestinal epithelial cells on the absorption process of SG and S. After oral administration of antibiotics in Sprague-Dawley rats, the reduced bacterial enzyme formation significantly hinders the absorption of SG, whereas scarcely that of S. The absorption study in situ single-pass intestinal perfusion revealed that S could be absorbed throughout the intestine of rats. The effective intestinal permeability of S in the jejunum was much lower than in the other sections of the GI tract. The efflux transporter promoted SG secretion into lumen from enterocytes, which hindered the absorption of both SG and S into the bloodstream. The efflux transporter protein inhibitor (verapamil, probenecid and reserpine) remarkably enhanced the absorption of S and the bioconversion of S into SG in both the rat intestine and Caco-2-monolayer models.

[Effect of Qufeng Tongluo Recipe on expression of desmin and CD2AP proteins in adriamycin-induced nephropathy rats: an experimental research].

OBJECTIVE: To investigate the effect of Qufeng Tongluo Recipe (QTR) on the expression of desmin and CD2-associated protein (CD2AP) in adriamycin-induced nephropathy rats. METHODS: The adriamycin-induced nephropathy rat model was induced by a disposable intravenous injection of adriamycin. The model was successfully established after 3 weeks. Rats were then randomly divided into the blank control group (Group A, n =12), the model control group (Group B, n = 8), the small, medium, large dose QTR group (Group C, n = 8; Group D, n = 8; Group E, n = 8), and the positive control group (Group F, n = 8). From the fourth week normal saline was given to rats in Group A and Group B, QTR 1.0 g/mL, 2.1 g/mL, and 4.2 g/mL was respectively administered to those in Group C, D, and E. Prednisone 25 mg/kg was given to rats in Group F. All medication was performed by gastrogavage at 10 mL/kg, once daily, for 28 successive days. 24-h urinary protein excretion and sera biochemical indices were determined during medication. At the end of the experiment, ultrastructure was observed, mRNA expression of desmin, mRNA and protein of CD2AP were detected by Real-time PCR and Western blot. RESULTS: (1) Compared with Group B, 24-h urinary protein excretion significantly decreased in Group C, D, E, and F (P < 0.05). (2) Compared with Group B, Alb in Group C, D, and E increased (P < 0.05) and TC significantly decreased (P < 0.05). TG significantly increased in Group F (P < 0.05). (3) Results of electron microscope showed, compared with Group B, the morphology of foot cells was improved to various degrees in Groups D, E, and F, especially the foot process structure and the number of foot processes were significantly improved, which was more obviously shown in Group D and Group E. (4) mRNA expression of desmin, mRNA and protein of CD2AP increased in adriamycin-induced nephropathy rats (P < 0.05). After intervention, when compared with Group B, mRNA expression of desmin and CD2AP were significantly lower in Group C, D, E, and F (P < 0.05). (5) Compared with Group A, expression of desmin and CD2AP significantly increased (P < 0.05). Compared with Group B, the expression of desmin protein were obviously lower in Group C, D, E, and F, and the protein expression of desmin obviously decreased in Group D, E, and F (P < 0.05). The protein expression of desmin and CD2AP gradually decreased in Group C, D, and E (P < 0.05). Compared with Group F, the expression of CD2AP protein obviously increased in Group C and D (P < 0.05); the expression of CD2AP protein obviously decreased in Group E (P < 0.05); the expression of desmin protein was higher in Group C, D, and E (P < 0.05). CONCLUSION: QTR's therapeutic effect on adriamycin-induced nephropathy rats might be achieved through altered expression of desmin and CD2AP.

[Development of needle-thread integrative embedding needle].

The needle-thread integrative embedding needle consists of needle handle, needle core, thread, locker and needle guard. The thread is fixed in the core by the locker. With the needle inserted into acupoint, the locker is separated from the thread, while the thread is embedded directly into acupoint, to achieve one acupoint with one needle. This type of thread embedding needle is operated simply and safely without cross infection occurrence, easy to carry.

Pravastatin inhibits C-reactive protein generation induced by fibrinogen, fibrin and FDP in isolated rat vascular smooth muscle cells.

OBJECTIVE: The available evidence indicates that C-reactive protein (CRP) participates directly in atherosclerosis formation as an inflammatory molecule. Our previous investigation suggested that fibrinogen, fibrin and fibrinogen degradation products (FDP) produce a pro-inflammatory effect on vascular smooth muscle cells (VSMCs) through inducing CRP generation. In the present study, we observed the effect of pravastatin on CRP generation induced by fibrinogen, fibrin and FDP in rat VSMCs. METHODS: VSMCs from Sprague-Dawley rats were cultured. Fibrinogen, fibrin and FDP were used as stimulants for CRP generation. VSMCs were preincubated with pravastatin at 10, 30, 100 µM for 30 min prior to stimulation. CRP mRNA expression was studied by reverse transcription polymerase chain reaction (RT-PCR). CRP levels in the supernatant of VSMCs were measured by enzyme-linked immunosorbent assay (ELISA). CRP expression in VSMCs was examined with immunocytochemical staining. RESULTS: ELISA analysis showed that the pravastatin concentration-dependently reduced fibrinogen-, fibrin- and FDP-stimulated generation of CRP in VSMCs, with maximal inhibition of 56.6, 55.7 and 62.3%, respectively. Immunocytochemical staining and RT-PCR revealed that pravastatin inhibited protein and mRNA expression of CRP in VSMCs significantly. CONCLUSIONS: Pravastatin at the concentrations used in the present experiment has ability to relieve vascular inflammation and to restrain atherosclerotic processes via inhibiting the CRP production induced by fibrinogen, fibrin and FDP in VSMCs, which helps explain the beneficial effects of pravastatin on atherosclerosis.

Rosiglitazone inhibits angiotensin II-induced C-reactive protein production in human aortic endothelial cells through regulating AT(1)-ROS-MAPK signal pathway.

OBJECTIVE: Atherosclerosis is an inflammatory disease. As an inflammatory molecule, C-reactive protein (CRP) plays a direct role in atherogenesis. Our previous study confirmed that angiotensin II (Ang II) is capable of inducing CRP generation in human aortic endothelial cells (HAECs). The present study observed the effect of rosiglitazone on Ang II-induced CRP expression in HAECs and molecular mechanisms. METHODS: HAECs were cultured, and Ang II (10(-6) M) was used as a stimulant for the generation of CRP and reactive oxygen species (ROS). HAECs were preincubated with rosiglitazone at 1, 10, 100 µM for 18 h prior to the stimulation. mRNA and protein expressions were identified by reverse transcription polymerase chain reaction and Western blot, respectively. ROS production was observed by a fluorescence microscope. RESULTS: Pretreatment of HAECs with rosiglitazone prior to Ang II stimulation markedly downregulated Ang II-induced mRNA and protein expressions of CRP (maximal inhibition of 55.2 and 99.1 %, P < 0.001 vs. Ang II alone) and AT(1) (maximal inhibition of 66.4 and 90.5 %, P < 0.001 vs. Ang II alone) in a concentration-dependent manner, inhibited Ang II-stimulated ROS production (P < 0.01 vs. Ang II alone), and attenuated Ang II-induced phosphorylation of ERK1/2 and JNK (P < 0.001 vs. Ang II alone). Meanwhile, AT(1) receptor blocker losartan also reduced Ang II-stimulated ROS generation in HAECs (P < 0.001 vs. Ang II alone). CONCLUSIONS: Rosiglitazone at the concentrations used in the present experiment is able to inhibit Ang II-induced CRP generation in HAECs by regulating AT(1)-ROS-MAPK signal pathway. These results strengthen our understanding of the anti-inflammatory and anti-atherosclerotic effects of rosiglitazone.

Short-term effect of 0.01% atropine sulphate eye gel on myopia progression in children.

AIM: To investigate the effect of 0.01% atropine sulphate eye gel on myopia progression and axial elongation in a 6-month treatment in children. METHODS: Totally 185 children aged 6-12y with binocular myopia of 3.0 D or less in both eyes were enrolled in this prospective cohort study. The atropine group (n=125) received one drop of 0.01% atropine sulphate eye gel in each eye before bedtime daily. The control group included 60 matched children without drug intervention during the same period. The spherical equivalent and axial length was recorded at baseline and the sixth month of treatment. The efficacy was evaluated by the change of the spherical equivalent and axial length. Adverse events were also recorded. RESULTS: The average spherical equivalent and axial length at baseline were not statistically significant between the atropine group (-1.64±0.80 D, 24.13±0.76 mm) and the control group (-1.59±0.94 D, 24.06±0.77 mm, P>0.05). After 6mo, there was significantly difference in the spherical equivalent progression between the atropine and the control group (-0.27±0.33 vs -0.60±0.35 D, P<0.001), with a relative reduction of 55.0% in myopia progression. The increase in axial elongation in the atropine group was significantly less than control group (0.19±0.14 vs 0.26±0.14 mm, P<0.001), with a relative reduction of 26.9% in axial length. The 84.4% and 38.4% of the eyes progressed by less than 0.50 D and remained stable in the atropine group, compared with 51.7% and 4.2% in the control group. No adverse events were observed. CONCLUSION: Atropine sulphate eye gel 0.01% can slow down myopia progression and axial elongation in children with a 6-month treatment.

Rosiglitazone regulates c-reactive protein-induced inflammatory responses via glucocorticoid receptor-mediated inhibition of p38 mitogen-activated protein kinase-toll-like receptor 4 signal pathway in vascular smooth muscle cells.

C-reactive protein (CRP) activates toll-like receptor 4 (TLR4) to initiate inflammatory response involved in the pathogenesis of atherosclerosis through mitogen-activated protein kinase (MAPK) signal pathways. Rosiglitazone, a synthetic peroxisome proliferator-activated receptor γ (PPARγ) agonist, is considered to be an important inhibitor of the inflammatory response. The present study was to explore the effect of rosiglitazone on the CRP-induced inflammatory responses and the related signal pathway in vascular smooth muscle cells (VSMCs). The results showed that rosiglitazone reduced the expressions of proinflammatory cytokines, such as vascular endothelial growth factor-A and inducible nitric oxide synthase, and enhanced the expression or activation of anti-inflammatory transcription factors including PPARγ and glucocorticoid receptor (GR) in VSMCs in response to CRP. The further investigations indicated that rosiglitazone inhibited CRP-induced TLR4 expression and p38 MAPK phosphorylation in VSMCs, and TLR4 knockdown potentiated the inhibitory effects of rosiglitazone on vascular endothelial growth factor-A and inducible nitric oxide synthase expressions. In addition, GR antagonist RU486 but not PPARγ inhibitor GW9662 remarkably weakened the inhibitory effects of rosiglitazone on CRP-induced TLR4 expression and p38 phosphorylation in VSMCs. But GW9662 did not affect rosiglitazone-induced GR phosphorylation. These suggest that rosiglitazone exerts its anti-inflammatory effect through activating GR and subsequently inhibiting p38 MAPK-TLR4 signaling pathway in CRP-stimulated VSMCs.

[Expression of indoleamine 2, 3-dioxygenase and its correlation with prognosis in breast cancer patients].

OBJECTIVE: To investigate the expression of indoleamine 2, 3-dioxygenase (IDO) in breast cancer and its correlation with clinicopathologic factors and prognosis. METHODS: The expression of IDO, CD31, CD105 proteins in 40 specimens of breast cancer were assessed by immunohistochemistry. RESULTS: The overexpression rate of IDO in breast cancer was 67.5% (27/40), and expression of IDO was closely associated with clinical stage and lymph nodes metastasis. The disease-free survival rate in patients with IDO overexpression was not significantly lower than that in patients with negative or low expression of IDO (P > 0.05). Moreover, the expression of IDO was positively correlated with CD105-labeled microvessel density (r = 0.659, P < 0.05). CONCLUSIONS: Expression of IDO is associated with clinical stage and lymph nodes metastasis, and microvessel densitty. IDO expression may promote the growth and metastasis of breast cancer, probably via the increased agiogenesis. A larger sample study is needed to verify whether the prognosis of beast cancer is significantly correlated with IDO expression.

[Mechanism of Dahuang Zhechong pill against atherosclerosis induced by balloon angioplasty in rabbits].

OBJECTIVE: To study the mechanism of Dahuang Zhechong pill (DHZCP) against atherosclerosis induced by balloon angioplasty in rabbits. METHODS: Atherosclerosis model was established by the combination of balloon angioplasty-induced endothelial injury and high cholesterol feeding in rabbit. Male New Zealand rabbits were divided into six groups randomly: normal control, sham, model, positive control and two doses of DHZCP-treated groups. Rabbits in DHZCP-treated groups were intragastrically administered 0.9 and 1.8 g/kg DHZCP for 60 days respectively,and rabbits in positive control group were given 0.5 g/kg Danshen. MDA, NO levels and SOD activity in serum, and MPO activity in the vascular wall were determined with spectrophotometry. Expressions of proliferating cell nuclear antigen (PCNA) and BCL-2 in the vascular wall were detected by SP immuohistochemical technique. RESULTS: Compared with the model group, DHZCP significantly reduced serum MDA level and MPO activity in the vascular wall, increased serum NO level and SOD activity,and inhibited PCNA and BCL-2 expressions in the vascular wall. CONCLUSION: DHZCP inhibits the formation and development of atherosclerosis through anti-oxidative action, protecting endothelium from injury,inhibiting proliferation and promoting apoptosis of vascular smooth muscle cells.

[International standard ISO 22236 Traditional Chinese medicine-Thread-embedding acupuncture needle for single use: experience and recommendation].

The ISO 22236 Traditional Chinese medicine-Thread-embedding acupuncture needle for single use, as the first international standard (IS) in acupoint thread-embedding field, has been officially published by International Organization for Standardization (ISO) in 2020. The background of its development, difficulties and countermeasures in the process of development were reviewed, and the experience of standard development was summarized, aiming to provide methods and references for future IS development of acupuncture and moxibustion instruments. It is suggested that strengthening the discourse power in the process of IS development, increasing the compound talents cultivation for IS, valuing the importance of enterprises in the development of IS, and creating an advantageous environment for the development of IS are the keys to improve the level of standardization of acupuncture and moxibustion instruments and play a more important role in the IS development.

[Protective effect of total flavonoid of Herba Pyrolae on acute myocardial ischemic injury induced by isoproterenol in rats].

OBJECTIVE: To investigate the protective effect of total flavonoid of Herba Pyrolae (TFHP) on acute myocardial ischemic injury induced by isoproterenol in rats and the primary mechanisms. METHODS: Acute myocardial ischemic models were established by i. s. of isoproterenol. ECG of the rats were recorded, activities of creatine phosphokinase (CK), lactate dehydrogenase (LDH) and the superoxide dismutase (SOD), and the levels of malondialdehyde (MDA), NO and FFA in rat serum were determined, heart index were measured and histopathological changes of myocardium were observed. RESULTS: In comparison with model group, TFHP raised the height of T wave, reduced CK, LDH activities and FFA levels in serum, decreased heart index and relieved myocardial ischemic injury. The primary study of its mechanism showed that TFHP decreased MDA level, increased SOD activity and NO levels in the rat serum. CONCLUSION: TFHP has protective effect on acute myocardial ischemic injury possibly via antioxidation and increasing the release and production of NO.

Dexmedetomidine pretreatment protects the heart against apoptosis in ischemia/reperfusion injury in diabetic rats by activating PI3K/Akt signaling in vivo and in vitro.

Dexmedetomidine (DEX) exerts cardioprotection against ischemia/reperfusion injury. However, the precise mechanisms underlying this cardioprotective effect in diabetic rats are still not fully understood. The aim of the present study was to investigate the cardioprotective mechanism of DEX pretreatment on myocardial ischemia/reperfusion (I/R) injury in diabetic rats. A total of 25 streptozotocin-induced diabetic rats were equally randomized into five groups: i) Sham, ii) DEX (100 µg/kg); iii) myocardial I/R; iv) myocardial I/R+DEX (10 µg/kg); and v) myocardial I/R+DEX (100 µg/kg) groups. Primary cardiomyocytes were cultured in DEX for 1 h, and then oxygen and glucose deprivation (OGD)/R for 36 h. These results showed that pretreatment with DEX significantly decreased the I/R-induced size of the myocardial infarction, structural damage, morphological changes and apoptosis in myocardial cells, as well as levels of creatinine kinase, malondialdehyde and cardiac troponin I, and increased the I/R-induced superoxide dismutase activity in vivo and in vitro. Furthermore, immunohistochemical staining and western blot analysis revealed that DEX pretreatment significantly increased the I/R-induced expression levels of B-cell lymphoma 2 (Bcl-2), phosphorylated phosphoinositide 3-kinase (pPI3K) and pAkt, and significantly decreased those of pBcl-2 associated agonist of cell death, Bcl-2-associated X protein and cleaved caspase 3 in vivo and in vitro. In addition, all of these cardioprotective effects of DEX were reversed by yohimbine and LY294002 pretreatment. These results suggested that DEX pretreatment may activate the PI3K/Akt signaling pathway in an α2 adrenoceptor-dependent manner. DEX pretreatment may exert cardioprotective effects against myocardial ischemia/reperfusion injury in diabetic rats through the I/R-induced inhibition of cell apoptosis by activating the PI3K/Akt signaling pathway.

Long-term results of breast conservation in Chinese women with breast cancer.

Between July 1989 and December 2002, 172 women with Stage I/II breast cancer were treated by breast conservation therapy (BCT). All underwent quadrantectomy and axillary node clearance. Minimum follow-up was 5 years and 79 (52%) were followed for >10 years. At 5 years, local relapse-free and overall survival rates were 98.3% and 98.3%. The 10-year rates were 95% and 94%, respectively. The 10-year local recurrence rate was higher in patients with involved margins (33.3% versus 2.7%, p = 0.0272). Furthermore 10-year death rates in margin positive patients were higher (18.2% versus 2.5%, p = 0.0486). Excellent or good cosmetic results were achieved in 54%. BCT is a reasonable option for early stage breast cancer in Chinese women but margin status is the most important determinant of local recurrence. Negative margins are required for optimal local control and minimization of distant metastasis.

[Inhibitory effect of fenofibrate on angiotensin II-induced toll-like receptor 4 expression, myeloperoxidase activity and expression in RAW264.7 cells].

This study is to investigate the effect of fenofibrate on angiotensin II (Ang II)-induced toll-like receptor 4 (TLR4) expression, myeloperoxidase (MPO) activity and expression in murine macrophage line RAW264.7 cells and explore its anti-inflammatory mechanism. TLR4 and MPO mRNA levels were analyzed by RT-PCR, and TLR4 and MPO protein expressions were measured by Western blotting. MPO activity in the cell supernatant was assayed with colorimetry. The results showed that fenofibrate reduced Ang II-induced mRNA and protein expression of TLR4 and inhibited activity, mRNA and protein expression of MPO in RAW264.7 cells in concentration-dependent manner. In addition, TLR4 blocker partially antagonized the effect of Ang II on MPO activity in RAW264.7 cells, and fenofibrate potentiated the inhibitory effect. Meanwhile, fenofibrate significantly suppressed LPS (TLR4 special ligand)-induced MPO activity in RAW264.7 cells. In conclusion, fenofibrate downregulated Ang II-induced TLR4 expression and blocked MPO secretion in RAW264.7 cells via interfering with the TLR4-dependent signaling pathway to alleviate inflammation, which might be one of its novel anti-inflammatory mechanisms.

Genistein inhibits Ang II-induced CRP and MMP-9 generations via the ER-p38/ERK1/2-PPARγ-NF-κB signaling pathway in rat vascular smooth muscle cells.

AIMS: C-reactive protein (CRP) and matrix metalloproteinase (MMP)-9 are involved in the inflammation of atherosclerosis lesions. Genistein (Gen) has been demonstrated to exert beneficial effect on the cardiovascular system. However, it remains unclear whether Gen produces anti-inflammatory effect in vascular smooth muscle cells (VSMCs). Therefore, we investigated the effects of Gen on CRP and MMP-9 expressions induced by angiotensin (Ang) II in VSMCs and the related molecular mechanism. MAIN METHODS: Rat VSMCs were cultured, and Ang II was used as a stimulant for CRP and MMP-9 expressions. CRP level was measured by ELISA. The mRNA and protein expressions of related indexes were identified by reverse transcription-polymerase chain reaction and western blot, respectively. KEY FINDINGS: Gen inhibited Ang II-stimulated CRP and MMP-9 mRNA and protein expressions in concentration- and time-dependent manners. Additionally, Gen ameliorated Ang II-induced p-ERK1/2, p-p38 and NF-κB expressions, antagonized Ang II-downregulated peroxisome proliferation-activated receptor (PPAR) γ and estrogen receptor (ER) ß expressions. After treating the VSMCs with GW9662 or ICI182780 in Gen treated groups, inhibitory effect of Gen on CRP and MMP-9 expressions were antagonized in Ang II-stimulated VSMCs. The treatment of VSMCs with ICI182780 abolished downregulations of p-p38/p-ERK1/2, and antagonized upregulation of PPARγ by Gen in Ang II-stimulated VSMCs. Moreover, the inhibitory effect of Gen on Ang II-stimulated NF-κB expression was abolished after preincubation of VSMCs with GW9662 in Gen treated groups. SIGNIFICANCE: Gen exerts anti-inflammatory property via the ER-p38/ERK1/2-PPARγ-NF-κB-CRP/MMP-9 signal pathway in Ang II-stimulated VSMCs.

Effect of Jinguo Weikang Capsule on proto-oncogene expression of gastric mucosa in rats with gastric precancerous lesions.

OBJECTIVE: To study the effect of Jinguo Weikang Capsule [see text] on the gene expression of H-ras, epidermal growth factor receptor (EGFR), P53 and C-myc of the gastric mucosa in rats with gastric precancerous lesions, and to investigate the action mechanism of JWC on gastric precancerous lesions. METHODS: A rat model with paratypical proliferation of the gastric epithelium mucosa was established by using 60Co irradiation. Rats were divided into the normal group, model group, high-, medium-, low-dose JWC treatment groups, and the vitacoenzyme control group, and were treated for 30 days. The expression of H-ras, EGFR, P53 and C-myc genes of the gastric mucosa was detected by using immunohistochemical methods. RESULTS: The expression and over-expression rates of H-ras, EGFR, P53 and C-myc gene in the high-and medium-dose JWC treatment groups were significantly lower (P<0.05) as compared with those of the model group. CONCLUSION: JWC can inhibit the expression of the H-ras, EGFR, P53 and C-myc genes expression of the gastric mucosa in rats, which may be one of mechanisms involved in suppressing or reversing gastric carcinogenesis.

[Progress in signal transduction pathways mediating effects of angiotensin II in endothelial cells].

Angiotensin II (Ang II) not only mediates the effects of vasoconstriction and blood pressure regulation, but is also implicated in inflammation, endothelial dysfunction, atherosclerosis, hypertension and congestive heart failure. Ang 1I activates pathways of MAPK, NADPH and ROS, non-receptor tyrosine kinases and receptor tyrosine kinases via AT1 receptor to produce various effects involved in regulation of endothelial functions, endothelial dysfunction and vascular inflammation response.

Angiotensin II-induced C-reactive protein generation: inflammatory role of vascular smooth muscle cells in atherosclerosis.

BACKGROUND: As the major target of Angiotensin II (Ang II) in the vessel wall, vascular smooth muscle cells (VSMCs) are a tentative source to produce C-reactive protein (CRP). However, it is largely unknown if Ang II is capable of inducing CRP production in VSMCs. METHODS AND RESULTS: Ang II induced a concentration-dependent release of CRP in cultured rat VSMCs as measured by sandwich ELISA. Real-time PCR revealed that Ang II significantly upregulated CRP mRNA level in vitro. Ang II-induced CRP generation in aortic VSMCs was also investigated using double-labeled fluorescent immunohistochemistry and in situ hybridization in subchronic Ang II administration in rats. Losartan but not PD123319 markedly blocked the Ang II-induced CRP production in cultured VSMCs, suggesting that such effect was mediated via Ang II type 1 receptor. Further, Western blotting analysis showed that mitogen-activated protein kinase (MAPK) activation was obligatory in Ang II-induced CRP production, since specific MAPK inhibitor PD098059 almost abolished the action. CONCLUSIONS: We identified that Ang II is capable of inducing CRP generation in VSMCs, in which Ang II type 1 receptor followed by MAPK signal pathway is involved. It strengthened the role of Ang II-induced CRP production by VSMCs in the inflammatory process in atherosclerosis.

In vitro inhibition of proliferation of vascular smooth muscle cells by serum of rats treated with Dahuang Zhechong pill.

Dahuang Zhechong pill (DHZCP) is a famous and classical Chinese herbal prescription, which is clinically used to treat hepatic, gynecological and cardiovascular diseases in China. The aim of this study was to observe the effects of the serum of rats treated with DHZCP on the proliferation of cultured rat vascular smooth muscle cells (VSMCs) stimulated by platelet-derived growth factor (PDGF), oxidized low density lipoprotein (ox-LDL) and hyperlipidemic serum (HLS), and on DNA, protein and collagen syntheses of VSMCs induced by PDGF in vitro. VSMCs proliferation was assayed by measuring the cell viability with MTT method, and syntheses of DNA, protein and collagen were evaluated by detecting [(3)H]-thymidine, [(3)H]-leucine and [(3)H]-proline incorporations, respectively. The results showed that PDGF, ox-LDL and HLS stimulated the proliferation of rat VSMCs in vitro. The serum of rats treated with DHZCP significantly inhibited the proliferation of rat VSMCs induced by the above stimulants and the incorporations of [(3)H]-thymidine, [(3)H]-leucine and [(3)H]-proline into rat VSMCs induced by PDGF in comparison with the model control group (P<0.01). The data suggest that DHZCP is able to obviously inhibit VSMCs proliferation via interfering with syntheses of DNA and protein, and to decrease production of extracellular matrix by VSMCs through antagonizing collagen synthesis.

[Protection of vascular endothelial cells from ox-LDL induced injury by protocatechualdehyde].

OBJECTIVE: To observe the protective effects of protocatechualdehyde on the human umbilical vein endothelial cells (CRL-1730) induced injury by ox-LDL. METHODS: The CRL-1730 were induced injury by ox-LDL, and then treated with protocatechualdehydes for 24 hours. The cytoactive of CRL-1730 was assessed by colorimetry of MTr, the NO level and NOS activity in the cell culture fluid were observed by colorimetry, and the expression of CD40 protein was determined by flow cytometry. RESULTS: Compared with the ox-LDL group, protocatechualdehyde increased,the number of CRL-1730 and the level of NO and NOS in cell culture fluid. Besides, protocatechualdehyde decreased the expression of CD40 protein, which was increased by ox-LDL. CONCLUSION: Protocatechualdehyde has protective effect on the CRL-1730 induced injury by ox-LDL and its mechanism of action may be related to the CD40/CD40L pathway.