Danggui Shaoyao San Ameliorates Renal Fibrosis via Regulation of Hypoxia and Autophagy

Danggui Shaoyao San (DSS), a traditional Chinese medicinal prescription, was widely used to reinforce earth to activate collaterals in ancient times. Recently, many clinical studies found that DSS had a renoprotection. In this study, we evaluated the effect of DSS on unilateral ureteral obstruction- (UUO-) induced renal fibrosis in rats and investigated the mechanisms underlying the effect. Sprague Dawley (SD) rats were randomized to UUO or Sham operation. After 1 day, the rats that underwent UUO were randomized to treatment for four experimental groups (n=10 each group): Sham, UUO only, UUO+ benazepril (Bena), and UUO+DSS. After 4 weeks, we demonstrated that DSS significantly suppressed UUO-induced renal hypertrophy by gravimetric. In addition, DSS obviously prevented UUO-induced disorder in renal structure and renal function by HE and biochemistry test. We also found that DSS abrogated UUO-induced renal fibrosis by Masson’s staining and collagen volume fraction (CVF) analysis; this is consistent with the western blot analysis that showed DSS abrogated the UUO-induced enhanced TGF-β1 and weakened BMP-7. Compared with the UUO only group, rats treated with DSS exhibited significant increase in vascular density, followed by decrease in hypoxia and HIF-1α protein level through western blot and immunofluorescence analysis. Furthermore, we also determined proteins of autophagy and DSS enhanced autophagy to prevent the damage-induced by UUO. Taken together, our findings demonstrated that DSS had a renoprotection effect in ameliorating renal fibrosis possibly via attenuating tissue hypoxia and regulating autophagy.

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Protective Effect of SIRT1 Activator on the Knee With Osteoarthritis

Frontiers in Physiology ◽

10.3389/fphys.2021.661852 ◽

2021 ◽

Vol 12 ◽

Author(s):

Zhenquan Zhou ◽

Zhenhan Deng ◽

Yuwei Liu ◽

Yizi Zheng ◽

Shiwei Yang ◽

...

Keyword(s):

Articular Cartilage ◽

Western Blot ◽

Volume Fraction ◽

Knee Joints ◽

Chondrocyte Apoptosis ◽

Control Group ◽

High Dose ◽

Sham Operation ◽

Significant Difference ◽

Sirt1 Activator

Osteoarthritis (OA), one of the most common chronic musculoskeletal disorders, is deemed to be correlated with aging. The SIRT1 activator, resveratrol, acts as a crucial regulator of aging and may have a potential therapeutic effect on OA. Rabbit OA models were established through destabilized medial meniscus surgery. A total of 40 healthy male New Zealand rabbits were divided into five groups: control group (sham operation), OA group, as well as low dose (LD), middle dose (MD), and high dose (HD) resveratrol-treated OA groups. 6 weeks after operation, 0.8 ml of normal saline was injected into the knee joints every other day in the control and OA groups, and 0.8 ml of 5, 10, and 15 μmol/L resveratrol was injected into the knee joints every other day in the LD, MD, and HD group, respectively. The rabbits were sacrificed 2 weeks after medication, and the articular cartilage of the knee joint was collected for Micro-CT, histology and Western blot analysis. Obvious articular cartilage lesion and joint space narrowing were detected in the OA group. Compared with the OA group, less osteoarthritic changes were observed in the MD and HD groups. The MD and HD groups had significantly lower bone volume fraction, trabecular number and Mankin scores than the LD and OA groups (p < 0.05). No significant difference was found between the OA and LD groups (p > 0.05). The expressions of SIRT1 and p53 detected by western blot were consistent with the aforementioned findings. Therefore, resveratrol can activate the SIRT1 gene to play a protective role in the OA process by inhibiting chondrocyte apoptosis, trabecular bone number increasing of the subchondral bone, as well as elevation of bone density. It demonstrated the importance of SIRT1 in maintaining articular cartilage health and provided a promising therapeutic intervention in the treatment of OA.

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Qingshen Buyang Formula Attenuates Renal Fibrosis in 5/6 Nephrectomized Rats via Inhibiting EMT and Wnt/β-Catenin Pathway

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2019/5370847 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9

Author(s):

Xueqin Zhang ◽

Jing Fang ◽

Zhiqiang Chen ◽

Bingwu Zhao ◽

Su Wu ◽

...

Keyword(s):

Signaling Pathway ◽

Renal Fibrosis ◽

Kidney Diseases ◽

Intragastric Administration ◽

Sham Operation ◽

Protective Effects ◽

Sprague Dawley ◽

Sham Operation Group ◽

Group 5 ◽

Underlying Mechanisms

As renal fibrosis significantly contributes to various kinds of chronic kidney diseases, this study aimed to investigate the renal protective effects of Qingshen Buyang Formula against renal fibrosis on 5/6 nephrectomized rats, and its underlying mechanisms were explored. A total of 24 male Sprague-Dawley rats were randomly divided into sham operation group (Sham group), 5/6 nephrectomy group (5/6Nx group), and Qingshen Buyang Formula treatment group (QBF group). The intervention was intragastric administration for 12 weeks. In the end, the blood samples were collected to test renal functional parameters, urine proteins were measured, and the left kidneys were removed for histological studies, as well as mRNA and protein expression analysis. The results showed that Qingshen Buyang Formula significantly decreased BUN, Scr, and proteinuria in 5/6Nx rats. Meanwhile, it ameliorated the kidney injury and fibrosis, exemplified by the depressed expression of collagen I and fibronectin (FN), which are the main components of ECM. Furthermore, the process of EMT inhibited the Wnt/β-catenin signaling pathway related genes, such as Wnt4, TCF4, β-catenin, and p-GSK3β. Collectively, the Qingshen Buyang Formula can improve renal function and attenuate renal fibrosis, and its underlying mechanisms may be related with inhibiting EMT and Wnt/β-catenin signaling pathway.

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Mesenchymal stem cells protect against obstruction-induced renal fibrosis by decreasing STAT3 activation and STAT3-dependent MMP-9 production

AJP Renal Physiology ◽

10.1152/ajprenal.00311.2016 ◽

2017 ◽

Vol 312 (1) ◽

pp. F25-F32 ◽

Cited By ~ 25

Author(s):

Futoshi Matsui ◽

Stephen A. Babitz ◽

Audrey Rhee ◽

Karen L. Hile ◽

Hongji Zhang ◽

...

Keyword(s):

Renal Fibrosis ◽

Smooth Muscle Actin ◽

Sham Operation ◽

Muscle Actin ◽

Sprague Dawley ◽

Renal Obstruction ◽

Sprague Dawley Rats ◽

Fibronectin Deposition ◽

Metalloproteinase 9

STAT3 is a transcription factor implicated in renal fibrotic injury, but the role of STAT3 in mesenchymal stem cell (MSC)-induced renoprotection during renal fibrosis remains unknown. We hypothesized that MSCs protect against obstruction-induced renal fibrosis by downregulating STAT3 activation and STAT3-induced matrix metalloproteinase-9 (MMP-9) expression. Male Sprague-Dawley rats underwent renal arterial injection of vehicle or MSCs (1 × 106/rat) immediately before sham operation or induction of unilateral ureteral obstruction (UUO). The kidneys were harvested after 4 wk and analyzed for collagen I and III gene expression, collagen deposition (Masson’s trichrome), fibronectin, α-smooth muscle actin, active STAT3 (p-STAT3), MMP-9, and tissue inhibitor of matrix metalloproteinases 1 (TIMP-1) expression. In a separate arm, the STAT3 inhibitor S3I-201 (10 mg/kg) vs. vehicle was administered to rats intraperitoneally just after induction of UUO and daily for 14 days thereafter. The kidneys were harvested after 2 wk and analyzed for p-STAT3 and MMP-9 expression, and collagen and fibronectin deposition. Renal obstruction induced a significant increase in collagen, fibronectin, α-SMA, p-STAT3, MMP-9, and TIMP-1 expression while exogenously administered MSCs significantly reduced these indicators of obstruction-induced renal fibrosis. STAT3 inhibition with S3I-201 significantly reduced obstruction-induced MMP-9 expression and tubulointerstitial fibrosis. These results demonstrate that MSCs protect against obstruction-induced renal fibrosis, in part, by decreasing STAT3 activation and STAT3-dependent MMP-9 production.

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Bitter Melon (Momordica charantia L.) Fruit Bioactives Charantin and Vicine Potential for Diabetes Prophylaxis and Treatment

Plants ◽

10.3390/plants10040730 ◽

2021 ◽

Vol 10 (4) ◽

pp. 730

Author(s):

Mahwish ◽

Farhan Saeed ◽

M. Sultan ◽

Ayesha Riaz ◽

Sagheer Ahmed ◽

...

Keyword(s):

Diabetes Management ◽

Health Care Systems ◽

Insulin Level ◽

Nutrition Therapy ◽

Health Claims ◽

Second Phase ◽

Bitter Melon ◽

Sprague Dawley ◽

Renal Hypertrophy ◽

Care Systems

Natural products are gaining clinical significance in modern day health care systems to prevent diseases. Bitter melon, a health promoting vegetable, is traditionally used for medical nutrition therapy to cure diabetes but to reap maximum health claims, vigilant control of its substances in diet is crucial as part of curative action for effective diabetes management. In the present research, first phase focused on detection of key bioactive components, i.e., charantin and vicine in different parts of its fruit. In the second phase, normal and hyperglycemic Sprague Dawley rats were fed on skin, flesh and whole fruit of bitter melon at 150 and 300 mg/kg body weight and assessed for diabetes prophylaxis and treatment. The highest amount of charantin (0.16 ± 0.02 mg/g) was recorded in flesh while vicine was present in abundance in whole fruit (0.21 ± 0.01 μg/100 g). In normal rats, bitter melon supplementation was helpful in managing the onset of diabetes. Hyperglycemic rats showed diabetic complications including polydipsia, polyuria, glycosuria, renal hypertrophy and increased glomerular filtration rate. However, bitter melon consumption showed significant improvements in these parameters. The most potent dose was 300 mg/kg whole fruit that resulted in 31.64% lowering of blood glucose level and 27.35% increase in insulin level in hyperglycemic rats.

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Conditioned medium-preconditioned EPCs enhanced the ability in oligovascular repair in cerebral ischemia neonatal rats

Stem Cell Research & Therapy ◽

10.1186/s13287-021-02157-4 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Ning Zhou ◽

Lei Wang ◽

Ping Fu ◽

Zihao Cui ◽

Yuhang Ge ◽

...

Keyword(s):

Endothelial Cells ◽

Western Blot ◽

Conditioned Medium ◽

Cognitive Outcome ◽

Adult Brain ◽

Neonatal Rat ◽

Vascular Density ◽

Cxcr4 Axis

Abstract Background Oligovascular niche mediates interactions between cerebral endothelial cells and oligodendrocyte precursor cells (OPCs). Disruption of OPC-endothelium trophic coupling may aggravate the progress of cerebral white matter injury (WMI) because endothelial cells could not provide sufficient support under diseased conditions. Endothelial progenitor cells (EPCs) have been reported to ameliorate WMI in the adult brain by boosting oligovascular remodeling. It is necessary to clarify the role of the conditioned medium from hypoxic endothelial cells preconditioned EPCs (EC-pEPCs) in WMI since EPCs usually were recruited and play important roles under blood-brain barrier disruption. Here, we investigated the effects of EC-pEPCs on oligovascular remodeling in a neonatal rat model of WMI. Methods In vitro, OPC apoptosis induced by the conditioned medium from oxygen-glucose deprivation-injured brain microvascular endothelial cells (OGD-EC-CM) was analyzed by TUNEL and FACS. The effects of EPCs on EC damage and the expression of cytomokine C-X-C motif ligand 12 (CXCL12) were examined by western blot and FACS. The effect of the CM from EC-pEPCs against OPC apoptosis was also verified by western blot and silencing RNA. In vivo, P3 rat pups were subjected to right common carotid artery ligation and hypoxia and treated with EPCs or EC-pEPCs at P7, and then angiogenesis and myelination together with cognitive outcome were evaluated at the 6th week. Results In vitro, EPCs enhanced endothelial function and decreased OPC apoptosis. Meanwhile, it was confirmed that OGD-EC-CM induced an increase of CXCL12 in EPCs, and CXCL12-CXCR4 axis is a key signaling since CXCR4 knockdown alleviated the anti-apoptosis effect of EPCs on OPCs. In vivo, the number of EPCs and CXCL12 protein level markedly increased in the WMI rats. Compared to the EPCs, EC-pEPCs significantly decreased OPC apoptosis, increased vascular density and myelination in the corpus callosum, and improved learning and memory deficits in the neonatal rat WMI model. Conclusions EC-pEPCs more effectively promote oligovascular remodeling and myelination via CXCL12-CXCR4 axis in the neonatal rat WMI model.

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Effects of TRPC6 Inactivation on Glomerulosclerosis and Renal Fibrosis in Aging Rats

Cells ◽

10.3390/cells10040856 ◽

2021 ◽

Vol 10 (4) ◽

pp. 856

Author(s):

Eun Young Kim ◽

Stuart E. Dryer

Keyword(s):

Renal Function ◽

Protective Effect ◽

Renal Fibrosis ◽

Transient Receptor Potential ◽

Smooth Muscle Actin ◽

Receptor Potential ◽

Sprague Dawley ◽

Age Related ◽

Sprague Dawley Rats ◽

Transient Receptor

Canonical transient receptor potential 6 (TRPC6) channels have been implicated in familial and acquired forms of focal and segmental glomerulosclerosis (FSGS) in patients and animal models, as well as in renal fibrosis following ureteral obstruction in mice. Aging also evokes declines in renal function owing to effects on almost every renal compartment in humans and rodents. Here, we have examined the role of TRPC6 in driving inflammation and fibrosis during aging in Sprague-Dawley rats. This was assessed in rats with non-functional TRPC6 channels owing to CRISPR-Cas9 deletion of a portion of the ankyrin repeat domain required for the assembly of functional TRPC6 channels (Trpc6del/del rats). Wild-type littermates (Trpc6wt/wt rats) were used as controls. Animals were evaluated at 2 months and 12 months of age. There was no sign of kidney disease at 2 months of age, regardless of genotype. However, by 12 months of age, all rats examined showed declines in renal function associated with albuminuria, azotemia and increased urine excretion of β2–microglobulin, a marker for proximal tubule pathology. These changes were equally severe in Trpc6wt/wt and Trpc6del/del rats. We also observed age-related increases in renal cortical expression of markers of fibrosis (α-smooth muscle actin and vimentin) and inflammation (NLRP3 and pro-IL−1β), and there was no detectable protective effect of TRPC6 inactivation. Tubulointerstitial fibrosis assessed from histology also appeared equally severe in Trpc6wt/wt and Trpc6del/del rats. By contrast, glomerular pathology, blindly scored from histological sections, suggested a significant protective effect of TRPC6 inactivation, but only within the glomerular compartment.

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The Protective Effect of Low-Dose Ethanol on Myocardial Fibrosis through Downregulating the JNK Signaling Pathway in Diabetic Rats

Journal of Diabetes Research ◽

10.1155/2016/3834283 ◽

2016 ◽

Vol 2016 ◽

pp. 1-7 ◽

Cited By ~ 4

Author(s):

Ying Yu ◽

Xian-Jie Jia ◽

Wei-ping Zhang ◽

Ting-ting Fang ◽

Jie Hu ◽

...

Keyword(s):

Mrna Expression ◽

Myocardial Fibrosis ◽

Low Dose ◽

Volume Fraction ◽

Diabetic Rats ◽

Heart Weight ◽

Hemodynamic Parameters ◽

Sprague Dawley ◽

Jnk Pathway ◽

Ethanol Feeding

Objective. To investigate the effects of low dose ethanol feeding in diabetic rats and analyze its underlying mechanisms.Methods. Male Sprague-Dawley rats were divided into 4 groups: control (Con), diabetes at 4 weeks (DM4W), diabetes at 8 weeks (DM8W), and EtOH + DM8W. After 8 weeks, hemodynamic parameters were recorded and heart weight/body weight (H/B) and hydroxyproline (Hp) content in myocardium were measured. Morphology of collagen in myocardial tissue was observed with Masson’s trichrome staining method and collagen volume fraction (CVF) was analysed. The mRNA expression of ALDH2 was assessed with Real-Time PCR. The protein expressions of p-JNK and JNK were evaluated using western blot.Results. In contrast to Con group, there was no difference in hemodynamic parameters in DM4W group, but mean arterial pressure and heart rate were decreased in DM8W group, and the ratios of H/B, Hp, and CVF were markedly increased. ALDH2 mRNA expression was decreased, while the ratio of p-JNK/JNK were increased. Compared with DM8W group, the above indexes were improved in EtOH + DM8W group.Conclusion. With low dose ethanol intervention, enhanced ALDH2 expression can antagonize the happening of myocardial fibrosis in diabetic rats, which may be relevant with downregulating the JNK pathway.

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Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with18F-Fluorodeoxyglucose MicroPET

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/507091 ◽

2013 ◽

Vol 2013 ◽

pp. 1-9 ◽

Cited By ~ 4

Author(s):

Jin-hui Li ◽

Jing Lu ◽

Hong Zhang

Keyword(s):

Cerebral Ischemia ◽

Rat Model ◽

Neurological Deficit ◽

Neuronal Maturation ◽

Vascular Density ◽

Sham Operation ◽

Therapeutic Effects ◽

Neuroprotective Effects ◽

Neuronal Marker ◽

Cerebral Ischemic

Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of18F-fluorodeoxyglucose (18F-FDG) micro positron emission tomography (microPET).Method. Middle cerebral artery occlusion was used to establish cerebral ischemia. Rats were divided into 5 groups: sham operation, cerebral ischemia-reperfusion untreated (CIRU) group, Scu-25 group (Scu 25 mg/kg/d), Scu-50 group (Scu 50 mg/kg/d), and nimodipine (10 mg/Kg/d). The treatment groups were given for 2 weeks. The therapeutic effects in terms of cerebral infarct volume, neurological deficit scores, and cerebral glucose metabolism were evaluated. Levels of vascular density factor (vWF), glial marker (GFAP), and mature neuronal marker (NeuN) were assessed by immunohistochemistry.Results. The neurological deficit scores were significantly decreased in the Scu-50 group compared to the CIRU group (P<0.001).18F-FDG accumulation in the ipsilateral cerebral infarction increased steadily over time in Scu-50 group compared with CIRU group (P<0.01) and Scu-25 group (P<0.01). Immunohistochemical analysis demonstrated Scu-50 enhanced neuronal maturation.Conclusion.18F-FDG microPET imaging demonstrated metabolic recovery after Scu-50 treatment in the rat model of cerebral ischemia. The neuroprotective effects of Scu on cerebral ischemic injury might be associated with increased regional glucose activity and neuronal maturation.

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A dose-escalating toxicology study of the candidate biologic ELP-VEGF

Scientific Reports ◽

10.1038/s41598-021-85693-6 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Jamarius P. Waller ◽

Stephen P. Burke ◽

Jason Engel ◽

Alejandro R. Chade ◽

Gene L. Bidwell

Keyword(s):

Growth Rate ◽

Renal Fibrosis ◽

Renal Diseases ◽

Tumor Growth Rate ◽

Vascular Density ◽

Tumor Vascularity ◽

Sd Rats ◽

Renal Vascular ◽

Dose Dependent ◽

Dose Escalating

AbstractVascular Endothelial Growth Factor (VEGF), a key mediator of angiogenesis and vascular repair, is reduced in chronic ischemic renal diseases, leading to microvascular rarefaction and deterioration of renal function. We developed a chimeric fusion of human VEGF-A121 with the carrier protein Elastin-like Polypeptide (ELP-VEGF) to induce therapeutic angiogenesis via targeted renal VEGF therapy. We previously showed that ELP-VEGF improves renal vascular density, renal fibrosis, and renal function in swine models of chronic renal diseases. However, VEGF is a potent cytokine that induces angiogenesis and increases vascular permeability, which could cause undesired off-target effects or be deleterious in a patient with a solid tumor. Therefore, the current study aims to define the toxicological profile of ELP-VEGF and assess its risk for exacerbating tumor progression and vascularity using rodent models. A dose escalating toxicology assessment of ELP-VEGF was performed by administering a bolus intravenous injection at doses ranging from 0.1 to 200 mg/kg in Sprague Dawley (SD) rats. Blood pressure, body weight, and glomerular filtration rate (GFR) were quantified longitudinally, and terminal blood sampling and renal vascular density measurements were made 14 days after treatment. Additionally, the effects of a single administration of ELP-VEGF (0.1–10 mg/kg) on tumor growth rate, mass, and vascular density were examined in a mouse model of breast cancer. At doses up to 200 mg/kg, ELP-VEGF had no effect on body weight, caused no changes in plasma or urinary markers of renal injury, and did not induce renal fibrosis or other histopathological findings in SD rats. At the highest doses (100–200 mg/kg), ELP-VEGF caused an acute, transient hypotension (30 min), increased GFR, and reduced renal microvascular density 14 days after injection. In a mouse tumor model, ELP-VEGF did not affect tumor growth rate or tumor mass, but analysis of tumor vascular density by micro-computed tomography (μCT) revealed significant, dose dependent increases in tumor vascularity after ELP-VEGF administration. ELP-VEGF did not induce toxicity in the therapeutic dosing range, and doses one hundred times higher than the expected maximum therapeutic dose were needed to observe any adverse signs in rats. In breast tumor—bearing mice, ELP-VEGF therapy induced a dose-dependent increase in tumor vascularity, demanding caution for potential use in a patient suffering from kidney disease but with known or suspected malignancy.

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Abstract 620: Chronic Allium Bakeri Intake Alleviated Hypertension and Aortic Media Thickness in 2-Kidney, 1-Clip Rats.

Hypertension ◽

10.1161/hyp.60.suppl_1.a620 ◽

2012 ◽

Vol 60 (suppl_1) ◽

Author(s):

Saori Kitamura ◽

Hiroko Hashimoto ◽

Yukiko Segawa ◽

Nobutaka Kurihara

Keyword(s):

Renovascular Hypertension ◽

Transient Receptor Potential ◽

Control Diet ◽

Receptor Potential ◽

Left Renal Artery ◽

Sham Operation ◽

Sprague Dawley ◽

Media Thickness ◽

Freeze Dried ◽

Aortic Media

Objective: Allium bakeri (AB) known as “rakkyo” and Allium sativum known as “garlic” contain alliin. Alliin easily turns into allicin, which is reported to decrease blood pressure (BP) through activating the excitatory ion channel transient receptor potential ankyrin-1. Thus, it is suggested that these vegetable decrease BP. Actually, garlic is reported to decrease BP and aortic media thickness in hypertensive animal models. However, it is practically difficult that garlic shows the effects, because it can hardly be eaten without heating and allicin is thermolabile. On the other hand, AB is usually eaten without heating. Therefore, in this study, we tested whether AB intake alleviates hypertension and aortic media thickness in hypertensive rats. Method: We used 2-kidney, 1-clip (2K1C) renovascular hypertension model. Male Sprague-Dawley rats (6 wo) were treated with sham operation (SHAM) or clipping the left renal artery (2K1C). After surgery, SHAM and 2K1C rats were respectively divided into 2 groups, which received a control diet (CONT) or a diet containing 1.0 % (w/w) freeze-dried AB powder for 7 weeks (AB). The systolic BP (SBP) was measured by a tail-cuff method every week. At the end of the protocol, mean arterial BP (MAP) was measured in each rat under anesthesia. Then, thoracic aorta was removed and the section of aorta was stained with hematoxylin and eosin. Results: From the 2nd week after surgery until the end of the protocol, SBP in 2K1C-CONT went up significantly compared with SHAM-CONT (174 ± 7 vs 120 ± 5 mmHg, at the end of the protocol, P < 0.01). However, SBP in 2K1C-AB did not go up through the protocol (127 ± 7 mmHg, P < 0.01 with 2K1C-CONT, at the end). In addition, the AB diet showed no significant effects on SBP in SHAM. These observations in SBP were similar to in MAP at the end of the protocol. The aortic media thickening was observed in 2K1C-CONT compared with SHAM-CONT. In 2K1C-AB, the thickness was significantly decreased compared with 2K1C-CONT, and was not significantly different from that in SHAM-AB. There were not significant differences between SHAM-CONT and SHAM-AB. Conclusion: Chronic intake of Allium bakeri, which can be eaten without heating, alleviated hypertension and aortic media thickness in rats with renovascular hypertension.

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