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Objective:To systematically evaluate the efficacy and safety of modified Buyang Huanwu Tang in the treatment of chronic heart failure. Method:CNKI database，Wanfang database，VIP database，Pubmed，MEDLINE，EMBASE and Cochrane database were retrieved systematically. The literature retrieval period is from no limit to December 2019，with "Buyang Huanwu Tang" and "chronic heart failure" "heart failure" as the key words for full-text retrieval of Chinese and English databases. Literatures of randomized controlled trials（RCTs） for chronic heart failure were included， and the data were extracted. Cochrane system evaluation method was used to score the quality of literature. Stata 14.0 was applied in Meta-analysis on the retrieval results. TSA0.9 was applied in test sequential analysis. Sensitivity analysis was made to explain heterogeneity，and funnel chart was used to evaluate publication bias. Result:A total of 2 037 patients were included in 21 RCT studies. The article quality risk assessment was generally unclear risk of bias. The results of meta-analysis showed that the left ventricular ejection fraction （LVEF） in the experimental group was significantly higher than that in the control group，with statistically significant differences ［MD=0.901，95% CI （0.772，1.029），P<0.01］，the left ventricular end diastolic diameter （LVEDd） in the experimental group was significantly lower than that in the control group，with statistically significant differences ［OR=-0.650，95% CI=（-0.854，-0.446），P<0.01］，BNP in the experimental group was significantly lower than that in the control group，with statistically significant differences ［MD=-1.212，95% CI=（-1.359，-1.066），P<0.01］，6-minute walk test （6MWT） in the experimental group was significantly higher than that in the control group，with statistically significant differences ［MD=0.797， 95% CI=（0.447，1.146），P<0.01］，and the effective rate in the experimental group was significantly improved，with statistically significant differences ［OR=1.840，95% CI=（1.680，2.016），P<0.01］. Conclusion:Modified Buyang Huanwu Tang combined with conventional western medicine treatment of chronic heart failure is more effective than single administration of western medicine treatment，and can improve clinical efficacy， effectively improve the LVEF of patients with chronic heart failure，reduce the LVEDd reduces plasma BNP levels，prolong the 6-minute walking distance，and reduce the incidence of adverse reactions.
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<b>Objective::To investigate the mechanism of Buyang Huanwu Tang (BYHWT) in improving synaptic structural plasticity after cerebral ischemia-reperfusion in rats. <b>Method::Middle cerebral artery occlusion and reperfusion model was established. SD rats were randomly divided into sham-operated group, model group, BYHWT group, BYHWT+ Gap26(connexin43 inhibitor)groups. BYHWT was given twice a day(16 g·kg<sup>-1</sup>), Gap26 was intraperitoneally injected once a day since the third day after surgery (25 g·kg<sup>-1</sup>). Brain was taken out at the 7<sup>th</sup> day. The changes of neuronal synaptic and gap junction ultrastructure were observed by transmission electron microscopy. Synaptophysin (SYN) and growth-associated protein-43 (GAP-43) protein expression were detected by Western blot and immunofluorescence. <b>Result::The structure of synapses was integrated, and the gap junctions were clear in sham-operated group. In the hippocampus of model group, the structure was destroyed, and the gap junctions disappeared. Compared with the sham-operated group, model group up-regulated the expressions of SYN and GAP-43 (<italic>P</italic><0.05, <italic>P</italic><0.01). In the hippocampus of BYHWT group, the structure was close to the normal. Furthermore, BYHWT up-regulated the expressions of SYN and GAP-43 (<italic>P</italic><0.05, <italic>P</italic><0.01). However, after the combined administration with Cx43 inhibitor (Gap26), the damage of synaptic structural decreased, only a small number of gap junctions with the structural integrity can be seen, and the effect of BYHWT on SYN and GAP-43 was inhibited (<italic>P</italic><0.05, <italic>P</italic><0.01). <b>Conclusion::BYHWT could improve the hippocampal synaptic structural plasticity obviously after the CIRI. The mechanism may be related to the increase of the expression of Cx43 and the promotion of the intervention of SYN and GAP-43.
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Objective::To observe the clinical efficacy of modified Buyang Huanwu Tang on patients with lumbar disc herniation (LDH) after percutaneous foramen endoscopy by the collateral disease theory, and its effect on inflammatory factors and pain-inducing mediators. Method::One hundred and forty-four patients were randomly divided into control group (72 cases) and observation group (72 cases) by random number table. Both groups’ patients were treated with percutaneous endoscopic lumbar discectomy(PELD), and symptomatic treatment dehydration and anti-inflammation were also given to those patients after the operation. Patients in observation group got modified Buyang Huanwu Tang, 1 dose/day. The course of treatment was 4 weeks, and a 12-week fellow-up was recorded. Before the operation and at the 3rd day, the 4th and 16th week after the operation, scores of visual analogue score of pain degree (VAS) were recorded. And before the operation and at the 1st, 4th and 16th week after the operation, scores of dysfunction index (ODI) of Oswestry were recorded. Failed back surgery syndrome of LDH was recorded during 16 weeks after the operation. And Japanese orthopaedic association (JOA) and Qi deficiency and blood stasis syndrome were scored. And the levels of prostaglandin E2 (PGE2), thromboxane B2 (TXB2), interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and serotonin (5-HT) were all detected, and the effect was assessed by improved Macnab. Result::At the 1st day and the 1st, 4th and 16th week after treatment, scores of VAS were all lower than those in control group (P<0.01). And at the 1st, 4th and 16th week after treatment, scores of ODI were lower than those in control group (P<0.01). The rate of incidence was 18.06%(13/72), which was lower than 37.5%(27/72) in control group (χ2=6.784, P<0.01). Scores of the total JOA and subjective symptoms, objective signs and daily activities were all higher than those in control group (P<0.01). And scores of symptom scores and total scores of deficiency and blood stasis syndrome were all lower than those in control group (P<0.01). After treatment, levels of TNF-α, IL-1β, PGE2, TXB2 and 5-HT were lower than those in control group (P<0.01). According to the rank sum test, the effect of modified Macnab was better than that in control group (Z=2.151, P<0.05). Conclusion::Based on Luobing theory, modified Buyang Huanwu Tang can alleviate pain and other symptoms, promote the recovery of lumbar vertebral function, inhibit the expressions of inflammatory factors and pain-causing mediators, alleviate the residual symptoms after recent operation, reduce the incidence of FBSS, promote the rehabilitation of patients after operation, and improve the efficacy.
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Objective::To explore the effect of Naoxintong ethanol extract (NXT) on pyroptosis of BV2 microglia cells induced by lipopolysaccharide (LPS), and to explain the mechanism of pyroptosis based on NOD like receptor thermoprotein domain 3 (NLRP3)/cysteine-proteinase-1 (Caspase-1) pathway. Method::BV2 cells was treated with different concentrations of NXT(2, 10, 50 mg·L-1) after induced by LPS(1 mg·L-1) in vitro. Real-time PCR was used to detect mRNA expression of pro-inflammatory cytokine such as interleukin 1 beta (IL-1β), tumor necrosis factor (TNF)-α, and NLRP3.Western bolt and immunofluorescence were used to observe the protein expression of NLRP3/Caspase-1 signaling pathway. Result::Compared with control group, after LPS(1 mg·L-1) stimulation, BV2 cells viability was decreased. The mRNA expression levels of IL-1β, TNF-α and NLRP3 were significantly elevated(P<0.01), the protein levels of NLRP3 and Caspase-1 p20/Caspase-1 were also increased. After given NXT(2, 10, 50 mg·L-1), BV2 cells viability reversed which induced by LPS. Compared with LPS group, the mRNA expression of IL-1β, TNF-α and NLRP3 reduced obviously with given 50 mg·L-1NXT (P<0.05, P<0.01), significantly inhibited NLRP3 high protein expression and Caspase-1 p20/Caspase-1 expression(P<0.01). Conclusion::NXT can inhibit LPS induced pyroptosis of BV2 cells and the mechanism may closely related to NLRP3/Caspase-1 signaling pathway.
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Objective::To observe the clinical efficacy of modified Buyang Huanwu Tang combined with Sanrentang in treating early diabetic nephropathy(DN)with deficiency of spleen and kidney, damp-heat and blood stasis syndrome and its effect on glucose and lipid metabolism, oxidative stress and inflammatory factors, in order to explore its mechanism. Method::A total of 72 early DN atients were randomly divided into control group and treatment group, with 36 cases in each group. The control group was orally treated with losartan potassium tablets(50 mg every time, once/day), while the treatment group was treated with modified Buyang Huanwu Tang combined with Sanrentang orally in addition to the therapy of the control group(1 dose/day). Both groups were treated for 3 months. The changes in clinical efficacy and safety indicators were observed for both groups. The 24 h urine albumin excretion rate(UAER), serum creatinine(SCr), serum cystatin C(Cys C), urea nitrogen (BUN), fasting blood glucose (FBG), 2 h postprandial blood glucose (2 hPG), glycosylated hemoglobin (HbA1c), total cholesterol (TC), triglyceride(TG), low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol(HDL-C), malondialdehyde(MDA), superoxide dismutase(SOD), glutathione Peroxidase(GSH-Px), interleukin-2(IL-2), interleukin-4(IL-4), interleukin-8(IL-8), interleukin-10(IL-10), tumor necrosis factor-α(TNF-α)of patients in two groups were observed before and after treatment. Result::The total clinical effective rate was 88.9%in therapy group, which was higher than 61.1%in control group(P<0.05). After treatment, levels of UAER, SCr, Cys C and BUN were lower in both groups(P<0.05), and the levels in treatment group were all lower than those in control group(P<0.05). Levels of FBG, 2 hPG and HbA1c were lower in both groups(P<0.05). There was no significant difference in FBG, 2 hPG and HbA1c levels between two groups after treatment. The levels of HDL-C were higher in both groups(P<0.05), and the levels in treatment group were higher than that in control group(P<0.05). The levels of TC, TG and LDL-C were lower in both groups(P<0.05), and the levels in treatment group were all lower than those in control group(P<0.05). The level of MDA was lower in both groups(P<0.05), and the level in the treatment group was lower than that in control group(P<0.05). The levels of SOD and GSH-Px were higher in both groups(P<0.05), and the levels in the treatment group were all higher than those in the control group(P<0.05). Serum levels of IL-2, IL-8 and TNF-α were lower in both groups(P<0.05), and the levels in the treatment group were lower than those in control group(P<0.05). Serum levels of IL-4 and IL-10 were higher in both groups(P<0.05), and the levels in the treatment group was higher than those in control group(P<0.05). Conclusion::Modified Buyang Huanwu Tang combined with Sanrentang is effective and safe in the treatment of early DN with spleen and kidney deficiency, damp-heat and blood stasis syndrome. They can further improve renal function and lipid metabolism, inhibit oxidative stress reaction and regulate the secretion balance of inflammatory factors in early DN patients.
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Objective::To explore the effect and mechanisms of Buyang Huanwu Tang (BYHWT) on atherosclerotic plaque based on regulatory T cells (Treg) and inflammation. Method::Totally 50 ApoE knockout(ApoE-/-)mice aged 8 weeks were randomly divided into model group, low, medium, high-dose BYHWT groups, positive control group, and C57/BL mice were taken as control group. The model group and the BYHWT group were given high-fat diet for 12 weeks, while the control group was given normal diet. After successful modeling, BYHWT groups were given drugs (5, 10, 20 g·kg-1) through intragastric administration, the positive control group was given rapamycin (4 mg·kg-1), while the control group and the model group were given equal doses normal saline through intragastric administration for 4 weeks. Four weeks later, the mice were sacrificed. Manufactured paraffin sections were prepared for the aortic sinus of the heart. The plaque area was evaluated by hematoxylin and eosin (HE) staining, and the number of Treg cells in immunohistochemical staining plaque was detected. Blood was collected from eye canthus of mice, the expression of inflammatory factors in peripheral blood was detected by enzyme-linked immunosorbent assay (ELISA), and the forkhead box P3 (Foxp3) gene expression in peripheral blood was detected by Real-time fluorescent quantitative polymerase chain reaction (PCR). Result::Compared with the control group, the area of atherosclerotic plaques in the model group was significantly increased (P<0.01), the contents of serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly increased (P<0.05), and transforming growth factor-β (TGF-β) and interleukin-10 (IL-10) were significantly decreased (P<0.05), and the peripheral blood Fxop3 mRNA expression was decreased (P<0.05). Compared with the model group, the plaque areas in middle-dose and high-dose BYHWT groups were significantly reduced(P<0.05), the peripheral blood TNF-α and IL-6 contents were decreased (P<0.01), the TGF-β and IL-10 expressions were increased in the high-dose group (P<0.05, P<0.01), the number of Treg cells in the plaque was increased in the high-dose group (P<0.01), and the peripheral blood Fxop3 mRNA expression was increased in each BYHWT group (P<0.01). Conclusion::BYHWT has an anti-atherosclerosis effect, which may be related to the increase of the number of Treg cells and thereby inhibiting the inflammatory response in vivo.
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Objective:To investigate the effects of Buyang Huanwu Tang （BHT） on axonal regeneration and neurological rehabilitation of the rats suffering ischemic stroke （IS）. Method:A total of 180 SD rats were used to establish a middle cerebral artery infarction （MCAO） model. The animals that were successfully modeled were randomly divided into model group， BHT group （12 g·kg-1） and nimodipine group （20 mg·kg-1）， and a sham group was established， with 28 rats in each group. After seven-days intragastric administration of BHT， the animals were sacrificed. TTC staining was used to test cerebral infarction. Brain water content was measured to observe cerebral edema. Bielschowsky's silver staining and immunofluorescence were performed to observe axonal degeneration and the protein expression of neurofilament protein-200（NF-200）. Quantitative real-time polymerase chain reaction （PCR） was used to analyze the mRNA expression of repulsion oriented molecule a （RGMa）， Ras homologous enzyme （Rho）， Rho kinase （ROCK）， and collapsion response regulatory protein 2 （CRMP2）. Neurological function scores assay was used to examine neurological recovery. Result:Compared with sham group， the cerebral infarction volume and brain water content increased significantly（P<0.01）， and motor function was markablely decreased in the model group. Axonal degeneration and nerve fiber damage were obviously observed. Also， gene expression of axon growth-related protein was deviation from normal （P<0.01）. Compared with model group， the cerebral infarction rate （P<0.01）， brain water content （P<0.01） and axonal degeneration of BHT group and nimodipine group were significantly reduced. The expression of NF-200 was increased. Also， the mRNA expression of RGMa， Rho and ROCK was lower （P<0.05） while the mRNA expression of CRMP2 was higher （P<0.01）. And the neurological function was significantly improved （P<0.05）. Conclusion:BHT can promote axon regeneration after ischemic stroke injury by regulating the mRNA expression of axon growth-related protein， thereby improving nerve function.
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Objective:To explore the neuroprotective effect and mechanism of Buyang Huanwu Tang (BYHWT) on experimental autoimmune encephalomyelitis (EAE) at different stages. Method:The 36 female C57BL/6 mice were immunized subcutaneously with myelin oligodendrocyte glycoprotein peptides (MOG35-55),then randomly divided into 9, 17, 28 d EAE control group. Each BYHWT group was orally given drugs on the 3rd day after immunization (50 g·kg-1·d-1), and EAE control group was given the same volume of normal saline in the same way once a day for 9, 17 and 28 d after immunization. The effect of BYHWT on EAE mice was observed with internationally accepted clinical score. Brain and spinal cord specimens were collected at 9, 17 and 28 d after immunization. The neuroprotective effect of BYHWT was observed by hematoxylin-eosin(HE)staining and solid blue staining (LFB). The expressions of BDNF and GAP-43 in spinal cord and brain were detected by Western blot. Result:After treatment, BYHWT can significantly inhibit myelitis cell infiltration and alleviate myelin loss. Compared with EAE group, the expression of Nogo-A in the spinal cord of each BYHWT group was significantly down-regulated (PPPPConclusion:BYHWT can improve the local nerve growth microenvironment and promote the expression of NTFs, reduce the expressions of neuroinhibitory factors, and play a role in neuroprotection.
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Objective:To investigate the molecular mechanism of Buyang Huanwu Tang in improving cerebral vasospasm after subarachnoid hemorrhage. Method:Eighty male Sprague-Dawley rats were randomly divided into sham operation group, model group, Buyang Huanwu Tang low and high dose (13, 26 g·kg-1·d-1) group. According to 10 mL·kg-1, the drug was administered twice a day for 7 days. The subarachnoid hemorrhage model was made by double occipital pool injection method. The neurological function scores of rats in each group were evaluated at 1, 3, 5 and 7 days. The diameter of basilar artery was measured by hematoxylin-eosin (HE)staining. The expressions of phosphp-phosphoinositide 3-kinases(p-PI3K), phosphp-protein kinase B(p-Akt),endothelial nitric oxide synthase(eNOS) and neuronal nitric oxide synthase(nNOS) protein in basilar artery brain tissue were detected by Western blot. The expression of nitric oxide(NO) and endothelin-1(ET-1) in rat cerebrospinal fluid was detected by enzyme-linked immunosorbent assay (ELISA). Result:Compared with sham operation group, the neurological function scores of the model group were significantly decreased (PPPPP-1·d-1) increased the neurological function scores 3 to 5 days after treatment, and the basilar artery diameter was significant increased (PPPPPPPPPConclusion:The protective effect of Buyang Huanwu Tang on cerebral vasospasm after subarachnoid hemorrhage may be related to up-regulation of p-PI3K, p-Akt and eNOS expression in PI3K/Akt/eNOS signaling pathway, thereby increasing NO production.
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Objective:To observe the effect of Yiqi Huoxue Tongmai method in treating lower extremity atherosclerotic disease (LEAD) and on hemodynamic index and vascular endothelial function. Method:One hundred and five patients were randomly divided into control group (52 cases) and observation group (53 cases) by random number table. Patients in control group were treated for controlling blood sugar, blood fat, blood pressure and given aspirin enteric-coated tablets, 100 mg/day, cilostazol tablets, 100 mg/day, 2 times/day. In addition to the therapy of control group, patients in observation group were given modified Danggui Sini Tang and Buyang Huanwu Tang for oral and washout, 1 dose/day. The treatment course lasted for 12 weeks. Before and after treatment, ankle brachial index (ABI) was detected. And intimal thickness of shallow femoral shallower, arteriae tibialis posterior and arteriae dorsalis pedis, hardening degree, patch size and degree of stenosis were detected by color Doppler ultrasound diagnostic apparatus. Qi deficiency and blood stasis syndrome were scored. And levels of the whole blood viscosity, plasma viscosity, erythrocyte sedimentation rate (ESR), D-dimer (D-D), fibrinogen (FIB), erythrocyte electrophoresis, fasting blood glucose (FPG), glycosylated hemoglobin (HbA1c), serum 25-hydroxyvitamin D3 ([25(OH)D3]), endothelin (ET), nitric oxide (NO) and homocysteine (Hcy) were detected. Result:By the rank sum test, the clinical effect in observation group was better than that in control group (Z=2.371, PPPPPP3] and NO were higher than those in control group (PConclusion:Modified Danggui Sini Tang and Buyang Huanwu Tang can ameliorate hemodynamics and vascular endothelial function, improve ABI, relieve arteriosclerosis and narrow degrees, and alleviate clinical symptoms.
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Objective:To investigate the effect of Buyang Huanwu Tang in resisting lipopolysaccharide (LPS)-induced macrophage activation and autophagy through phosphatidylinositol 3-kinase/protein kinase B/mammalian rapamycin target protein (PI3K/Akt/mTOR) signaling pathway. Method:The cell counting kit-8 (CCK-8) method was used to screen out the optimal LPS concentration for inducing the activity of RAW264.7 macrophages. RAW264.7 macrophages were treated separately with PI3K blocker 3-methyladenine(3-MA) (5 mmol·L-1), Akt blocker MK2206 (5 μmol·L-1), mTOR blocker Rapamycin (10 μmol·L-1), Beclin1 blocker Spautin-1 (5 μmol·L-1), different doses of Buyang Huanwu Tang serum (5%, 10%, 20%) and the optimum concentration of LPS for 24 h. The concentrations of inflammatory factors interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in RAW264.7 macrophages were detected by enzyme-lined immunosorbent assay(ELISA). Western blot was used to detect the expression levels of phosphorylated PI3K, phosphorylated Akt, phosphorylated mTOR protein, microtubule light chain protein 3 (LC3), ubiquitin-binding protein 1 (p62) and Beclin-1. The autophagy flow of RAW264.7 cells was detected by transfection with autophagy double-labeled adenovirus. Result:Results of CCK-8 showed the highest cell viability when 10 mg·L-1 LPS was applied. The concentrations of IL-1β, IL-6 and TNF-α in the model group were significantly higher than those in the blank group (PPβ, IL-6 and TNF-α (PPPPPPPPConclusion:Buyang Huanwu Tang can resist LPS-induced macrophages activation and autophagy, inhibit macrophage inflammatory response, regulate PI3K/Akt/mTOR signaling pathway, and inhibit the excessive occurrence of autophagy.
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Objective: To study the effect of Buyang Huanwu Tang on myocardial energy metabolism in rats with diastolic heart failure (DHF) based on adenosine monophosphate (AMP)-activated protein kinase (AMPK)/peroxisome proliferators-activated receptors α (PPARα) signaling pathway,and investigate its mechanism of action.Method: The 48 SD rats were randomly divided into sham operation group and model group.DHF rat model was established by abdominal aorta constriction method.The successfully modeled rats were randomly divided into model group,Buyang Huanwu Tang group (12.72 g·kg-1·d-1),metoprolol tartrate group (0.004 5 g·kg-1·d-1),with corresponding drugs in each group by intragastric administration.The sham operation group and model group were given with equal amount of deionized water,once a day.After 8 weeks of continuous drug intervention,the contents of adenosine monophosphate (AMP),adenosine diphosphate (ADP) and adenosine triphophate (ATP) in peripheral blood of rats were determined by enzyme linked immunosorbent assay (ELISA).The changes of myocardial mitochondrial ultrastructure were detected by electron microscope.The protein expression levels of AMPK,PPARα and peroxisome proliferator-activated receptor-γ coactivator-1α(PGC-1α) in rat myocardium were detected by Western blot.Result: As compared with sham operation group,the contents of AMP and ADP in model group were increased significantly,and ATP content was decreased significantly (PPPPα and PGC-1α protein in the model group were decreased significantly (Pα and PGC-1α protein in Buyang Huanwu Tang group and metoprolol tartrate group were increased significantly (PConclusion: Buyang Huanwu Tang may improve the energy metabolism of the failed heart and delay the progression of heart failure by improving the structure and function of mitochondria,activating AMPK and up-regulating the expression of AMPK/PPARα signaling pathway.
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Objective: To explore the changes and benefits of vascular endothelial cell function in rats with qi deficiency and blood stasis syndrome, and the effect of Yiqi Huoxue recipe (YQHXF) of such changes. Method: Rats were randomly divided into blank control group, Qi deficiency and blood stasis group, and YQHXF high and low dose groups (5.54,2.77 g·kg-1). A small platform of water environment was used to make the rats stand for a long-term with irregular and incomplete sleep deprivation, 16 h per day for six weeks, so that both mentality and labor of rats were consumed to establish qi deficiency and blood stasis rat models. From the fifth week, intragastric administration was given for 2 weeks, until end of the experiment. Then levels of endothelin-1(ET-1), von willebrand factor (vWF), vascular cell adhesion molecule-1(VCAM-1), intercellular adhesion molecule (ICAM-1), P-selectin,interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in rat plasma were detected by enzyme-linked immunosorbent assay (ELISA) and nitric oxide (NO) was detected by nitrate reductase assay. Result:Compared with blank control group, rats in Qi deficiency and blood stasis group showed rough and dark hair, with significantly decreased body weight and pulse amplitude (PPPα were abnormally increased after sleep deprivation (PPPPPPPConclusion:Sleep deprivation can induce the formation of Qi deficiency and blood stasis syndrome in rats, and lead to vascular endothelial dysfunction. YQHXF has the function of protecting the vascular endothelium. It can improve the Qi deficiency and blood stasis symptoms in rats with Qi deficiency and blood stasis syndrome by regulating the secretion of vascular endothelial active substances, reducing cell adhesion and inhibiting inflammation.
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Objective:To observe the expression of mammalian target of rapamycin (mTOR) that mediates autophagy in pulmonary fibrosis and the effect of autophagy in the formation of pulmonary fibrosis, in order to explore the treatment mechanism of Buyang Huanwu Tang on pulmonary fibrosis. Method:Totally 144 C57BL/6 mice were randomly divided into 6 groups:sham operation group, model group, prednisone group, high-dose Buyang Huanwu Tang group, medium-dose Buyang Huanwu Tang group and low-dose Buyang Huanwu Tang group, with 24 mice in each group. The sham operation group was injected with the same amount of 0.9% saline. The remaining groups were treated with bleomycin tracheal injection to replicate the pulmonary fibrosis model. After modeling, sham operation group and model group were given 0.9% normal saline (0.01 g·kg-1·d-1), group high-dose Buyang Huanwu Tang group was given Buyang Huanwu Tang (28.08 g·kg-1·d-1), medium-dose Buyang Huanwu Tang group was given Buyang Huanwu Tang (14.04 g·kg-1·d-1), low-dose Buyang Huanwu Tang group was given Buyang Huanwu Tang(7.02 g·kg-1·d-1), and P group was given prednisone (0.455 g·kg-1·d-1) by gavage. The samples were taken in batches on the 7th, 14th and 28th days after modeling; degrees of alveolitis and fibrosis in mice were observed by hematoxylin-eosin (HE) staining and Masson staining. The mTOR protein, ribosomal S6 protein and microtubule associate protein 1 hight chain3-Ⅱ(MAP1LC3-Ⅱ) of mouse lung tissue were detected by Western blot; electron microscopy was used to observe the autophagy of lung tissue in mice. Result:Compared with the sham-operated group, the degrees of alveolitis and pulmonary fibrosis were significantly severer in the model group on 7th, 14th and 28th days (PPPPConclusion:The mTOR protein is activated in mice lung tissue, autophagy is inhibited, mTOR protein participates in the pathogenesis of pulmonary fibrosis by inhibiting autophagy; Buyang Huanwu Tang has a certain therapeutic effect on BLM-induced pulmonary fibrosis in mice, and its mechanism may be related to the down-regulation of mTOR protein expression that mediates autophagy.
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Objective: To investigate the changes of serum proneurotensin (PNT) and insulin-like growth factor-1 (IGF-1) levels in patients with diabetic peripheral neuropathy (DPN) and their relationship with nerve conduction velocity (NCV) and Toronto Clinical Scoring System (TCSS), so as to observe the clinical efficacy of modified Buyang Huanwu Tang on DPN patients and its effect on the levels of PNT and IGF-1. Method: Totally 68 patients with DPN were randomly divided into treatment group and control group, with 34 cases in each group. Both groups were given mecobalamin capsules orally in addition to routine therapy of diabetes, while the treatment group was given modified Buyang Huanwu Tang orally for 4 weeks. The sensory nerve conduction velocity (SNCV) of median nerve, motor nerve conduction velocity (MNCV) of median nerve, SNCV of common peroneal nerve, MNCV of common peroneal nerve, TCSS score and serum PNT, IGF-1 levels were observed before and after treatment. Result: Before treatment, there was no significant difference in SNCV of median nerve, MNCV of median nerve, SNCV of common peroneal nerve, MNCV of common peroneal nerve, TCSS score and serum levels of PNT and IGF-1 between two groups. Serum levels of PNT and IGF-1 were positively correlated with SNCV of median nerve, MNCV of median nerve, SNCV of common peroneal nerve and MNCV of common peroneal nerve (PPPPPPPConclusion: Serum PNT and IGF-1 may be involved in the occurrence and progress of DPN in patients with diabetes mellitus. Modified Buyang Huanwu Tang can increase the levels of serum PNT, IGF-1, NCV but reduce TCSS score in patients with DPN. It has a definite curative effect on DPN.
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Alzheimer' s disease (AD) is a neurodegenerative disease with insidious onset and complex etiology and pathogenesis. The main pathological changes are the damage of cholinergic neurons and the loss of synapses. Because of advantages of multi-pathway and multi-target intervention, traditional Chinese medicine(TCM) compound prescriptions have a significant effect in the prevention and treatment of AD. Buyang Huanwu Tang, which is the representative prescription for benefiting Qi and activating blood circulation, has been widely used in cerebrovascular diseases, with significant effects in protecting neurons, repairing blood-brain barrier, reducing permeability, resisting cerebral edema and vascular endothelial cell injury and promoting new angiogenesis and maturation. Due to its powerful therapeutic effect the brain, a large number of scholars have found that Buyang Huanwu Tang has a significant effect in improving cognitive impairment, and different components can improve the therapeutic effect of cognitive impairment through different mechanisms. However, different studies focus on a relatively single mechanism of action, which is not conducive to a comprehensive understanding of its mechanisms of action and intervention targets. This article summarizes relevant literatures in recent years for the effect of Buyang Huanwu Tang and its component in reducing beta amyloid precursor protein (APP) expression and beta amyloid protein deposition, inhibiting the central nervous system inflammatory signaling pathways in reducing inflammatory cytokines release factor expression protect neurons, repair, neuron apoptosis blood brain barrier, preventing harmful substances from the central nervous system, improving the low-density lipoprotein receptor (LRP)-1 content, lowering ages receptor (RAGE) beta amyloid protein expression, and increasing peripheral clearance of β amyloid protein, and elaborated the mechanisms in protecting neurons and alleviating learning and cognitive dysfunction, in order to provide strong literature support for the treatment of Alzheimer's disease with Buyang Huanwu Tang.
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Objective:To investigate the regulatory effect of serum containing Buyang Huanwu Tang on endothelial-to-mesenchymal transition(EndMT) in human pulmonary artery endothelial cells (HPAEC), and make further analysis on its mechanism from the perspective of the signal transduction of Jagged1/Notch1. Method:Rabbit serum containing Buyang Huanwu Tang was prepared by gavage with dosage of 53.36 g·kg-1·d-1, and blank serum was prepared by gavage with same volume of normal saline. The HPAECs cultured in vitro, EndMT model was established by the transforming growth factor-β1(TGF-β1) induced, which were divided into five groups:the control group (10%blank serum), the model group (10%blank serum+TGF-β1), the serum containing high-dose Buyang Huanwu Tang group (10%medicated serum + TGF-β1), the medium-dose group (5%medicated serum + 5%blank serum medicated + TGF-β1) and the low-dose group(2.5%medicated serum+7.5%blank serum+ TGF-β1). Cell proliferation was detected by methyl thiazolyl tetrazolium (MTT) method. Cell migration was detected by transwell and scratch assay. The endothelial markers platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31), vascular endothelial cadherin (VE-cadherin) and the mesenchymal markers fibroblast-specific protein 1 (FSP1), α-smooth muscle actin (α-SMA) were observed by immunofluorescence assay. The expression levels of Notch1, Jagged1 and CBF1 were detected by Western blot assay. Result:Compared with the control group, the proliferation and migration abilities of the HPAEC cells in model group were enhanced (Pα-SMA were increased. Further study found that the expressions of Notch1, Jagged1 and CBF1 were up-regulated (PPPα-SMA were on the decline. The expressions of Notch1, Jagged1 and CBF1 were also significantly lower than those in model group (PPConclusion:The serum containing Buyang Huanwu Tang can partly inhibit the EndMT in human pulmonary artery endothelial cells, which may be related to the regulation effect of Jagged1/Notch1 signaling.
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Objective:To analyze and identify the brain and blood absorption components of rats after intragastric administration of Buyang Huanwu Tang(BYHWT). Method:The brain tissue,plasma of normal rats and the cerebral ischemia-reperfusion rats were analyzed by UPLC-Q-TOF-MS/MS.The prototype components in BYHWT were identified according to retention time,accurate relative molecular weight,primary and secondary mass spectrometry data. Result:After the administration of BYHWT,five compounds were found to enter the normal brain tissue through the blood-brain barrier and identified as calycosin-7-glucoside,albiflorin,formononetin-7-O-β-D-glucoside-6″-O-acetyl,safflower yellow A and astragaloside A;two compounds penetrated the blood-brain barrier and entered modeling brain tissue,and they were identified as calycosin-7-glucoside and formononetin-7-O-β-D-glucoside-6″-O-acetyl;seven compounds entered normal plasma and were identified as calycosin-7-glucoside,albiflorin,hydroxysafflor yellow A,et al;three compounds entered model plasma and identified as calycosin-7-O-β-D-glucoside-6″-O-acetyl,6″-O-acetyl-(6αR,11αR)-9,10-dimetho-xypterocarpan-3-O-β-D-glucoside and formononetin-7-O-β-D-glucoside-6″-O-acetyl. Conclusion:BYHWT has different pharmacological material basis in normal and cerebral ischemia-reperfusion rats.
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Object To study the isomers of amygdalin in BUYANG HUANWU TANG and its production Methods Amygdalin was isolated from both peach seeds and BUYANG HUANWU TANG by using various column chromatography Their structures were identified by the various spectral data Results Amygdalin had been isolated from n BuOH fraction of aqueous extract of BUYANG HUANWU TANG and found to be a pair of D , L epimers and their ration was 1∶1 It was also found that the structures and the ration of D , L epimers of amygdalin in decoction of single peach seed were similar to that in BUYANG HUANWU TANG. The peach seed only gave D amygdalin when it was extracted in 95% EtOH at reflux temperature, and D amygdalin cannot be isomerized when it was treated in water at 100 ℃ Conclusion Isomerization of D amygdalin results from interaction between it and other compounds of peach seed in water at high temperature, and has no evident relation to other constituents in BUYANG HUANWU TANG L amygdalin is a new compound generated due to decoction of peach seed