scholarly journals Plicosepalus acacia Extract and Its Major Constituents, Methyl Gallate and Quercetin, Potentiate Therapeutic Angiogenesis in Diabetic Hind Limb Ischemia: HPTLC Quantification and LC-MS/MS Metabolic Profiling

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1701
Author(s):  
Asmaa R. Abdel-Hamed ◽  
Eman T. Mehanna ◽  
Reem M. Hazem ◽  
Jihan M. Badr ◽  
Dina M. Abo-Elmatty ◽  
...  

Plicosepalus acacia (Fam. Loranthaceae) has been reported to possess hypoglycemic, antioxidant, antimicrobial, and anti-inflammatory effects. Liquid chromatography combined with tandem mass spectrometry (LC-MS/MS) analysis revealed the presence of a high content of polyphenolic compounds that are attributed to the therapeutic effects of the crude extract. In addition, methyl gallate and quercetin were detected as major phytomedicinal agents at concentrations of 1.7% and 0.062 g%, respectively, using high-performance thin layer chromatography (HPTLC). The present study investigated the effect of the P. acacia extract and its isolated compounds, methyl gallate and quercetin, on hind limb ischemia induced in type 1 diabetic rats. Histopathological examination revealed that treatment with P. acacia extract, methyl gallate, and quercetin decreased degenerative changes and inflammation in the ischemic muscle. Further biochemical assessment of the hind limb tissue showed decreased oxidative stress, increased levels of nitric oxide and endothelial nitric oxide synthase (eNOS), and enhancement of the levels of heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) in the groups treated with methyl gallate and quercetin. Expression levels of hypoxia inducible factor-1 alpha (HIF-1α), VEGF, fibroblast growth factor-2 (FGF-2), and miR-146a were upregulated in the muscle tissue of methyl gallate- and quercetin-treated groups along with downregulation of nuclear factor kappa B (NF-κB). In conclusion, P. acacia extract and its isolated compounds, methyl gallate and quercetin, mediated therapeutic angiogenesis in diabetic hind limb ischemia.

Hypertension ◽  
1999 ◽  
Vol 33 (6) ◽  
pp. 1379-1384 ◽  
Author(s):  
Ryuichi Morishita ◽  
Shigefumi Nakamura ◽  
Shin-ichiro Hayashi ◽  
Yoshiaki Taniyama ◽  
Atsushi Moriguchi ◽  
...  

Circulation ◽  
2001 ◽  
Vol 104 (19) ◽  
pp. 2344-2350 ◽  
Author(s):  
Yoshiaki Taniyama ◽  
Ryuichi Morishita ◽  
Kazuya Hiraoka ◽  
Motokuni Aoki ◽  
Hironori Nakagami ◽  
...  

2005 ◽  
Vol 280 (15) ◽  
pp. 14790-14798 ◽  
Author(s):  
Germana Zaccagnini ◽  
Carlo Gaetano ◽  
Linda Della Pietra ◽  
Simona Nanni ◽  
Annalisa Grasselli ◽  
...  

2002 ◽  
Vol 17 (1) ◽  
pp. 100-102 ◽  
Author(s):  
Tuomas T. Rissanen ◽  
Johanna E. Markkanen ◽  
Katja Arve ◽  
Juha Rutanen ◽  
Mikko I. Kettunen ◽  
...  

2012 ◽  
Vol 55 (6) ◽  
pp. 18S-19S
Author(s):  
Robert Brenes ◽  
Caroline C. Jadlowiec ◽  
Mackenzie Bear ◽  
Peter Hashim ◽  
Clinton D. Protack ◽  
...  

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
annamalai senthilkumar ◽  
Ray Smith ◽  
Jayant Khitha ◽  
John W Langston ◽  
John H. Chidlow ◽  
...  

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Alvaro F Manrique ◽  
Shyamal C Bir ◽  
Elvis Peter ◽  
Rui Wang ◽  
Christopher G Kevil

Introduction: Arteriogenesis is an important process involving remodeling of collateral vasculature during chronic or intermittent tissue ischemia. CSE and eNOS are the two principle enzymes for hydrogen sulfide (H 2 S) and Nitric Oxide (NO) generation. Although role of NO during arteriogenesis is partially known, the role of CSE dependent H 2 S production during arteriogenesis remains unknown. Hypothesis/objective: We sought to determine the role of CSE generated H 2 S on arteriogenesis activity of CSE knockout (CSEKO) mice compared to eNOS knock out (eNOSKO) and wild type (WT) mice during hind limb ischemia. Method: Permanent unilateral hind limb ischemia was induced in 12-week-old CSE KO, eNOS KO, and WT mice and studied until day 21. Tissue perfusion was measured using indicator dye blush rates with the SPY Imager system over time along with laser doppler flowmetry. Temporal development of arterial remodeling was also observed using SPY imaging, and vessel number, length and branch morphometry determined over time. Microfil vascular casting was performed to further examine the number of collaterals in ischemic muscles at the end of the study. Histological arteriogenesis was evaluated by vascular smooth muscle actin (SMA) positive vessel density with dual fluorescence staining of anti-CD31 (endothelial positive cell) and anti-α-SMA antibodies. Results: Tissue perfusion was significantly impaired in CSE KO and eNOS KO mice compared to WT mice at different time points throughout the study period. Both CSE KO and eNOS KO mice showed significantly less blush rate than WT mice. SMA positive vessel density was also significantly less in CSE KO and eNOS KO mice than that in WT mice. Conclusion: CSE generated H 2 S and eNOS derived NO play important roles in regulating ischemic arterial remodeling as demonstrated in our studies. The mechanism of impaired arteriogenesis in both mutant mice and the interaction between these two gasotransmitters has yet to be elucidated.


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