scholarly journals Nutritive diet becomes unhealthy if taken in a wrong ratio: Scientific validation of Ayurvedic concept of “incompatible diet” (Virrudh Aahar)

2019 ◽  
Author(s):  
Prerana Aditi ◽  
Shivani Srivastva ◽  
Harsh pandey ◽  
Y.B. Tripathi

AbstractHoney and ghee is an important constituent of our diet. Honey contain about 200 components in its which play an important role as antioxidative, anti-inflammatory, antimicrobial, wound healing and sunburn, etc. Ghee has also many essential constituents such as phospholipids, PUFA, fat- soluble vitamins, etc. It is mention in Charak Samhita that equal ratio of honey and ghee when taken in food become toxic to health. This study was designed to explore the mechanism of toxicity through the biochemical and histological parameter. For this study, 24 Charles foster rats were taken and divided into four groups (n=6) normal, honey, ghee, and honey+ghee (1:1). After 60 days rats were sacrificed. Weight loss, Hair loss and red patches on ear were found on honey+ghee fed rats. LFT, amadori test, AGE, UV, glucose, DPP-4 and LPO were found significantly increased in honey+ghee group. SOD, Catalase, GSH, ABTS+, GLP-1, GIP-1, ACB and HB were found significantly decreased in honey+ghee group. No changes were found in RFT. H&E show normal morphology in kidney, intestine, and pancreas but mild inflammation was found in liver tissue. We conclude that the equal mixture of honey and ghee shows toxic effect. Increased formation of hydroxymethyl furfural, amadori product, DPP-4 activity and low incretins (GLP-1, GIP-1) activity resulting high postprandial hyperglycemic response are collectively responsible for oxidative stress-mediated toxicity of the mixture of honey and ghee in equal ratio.


Author(s):  
Glêbia A. Cardoso ◽  
Mateus D. Ribeiro ◽  
Ana P. Ferreira ◽  
Yohanna de Oliveira ◽  
Thiago de O. Medeiros ◽  
...  


Drug Research ◽  
2020 ◽  
Author(s):  
Tina Didari ◽  
Shokoufeh Hassani ◽  
Maryam Baeeri ◽  
Mona Navaei-Nigjeh ◽  
Mahban Rahimifard ◽  
...  

Abstract Aim of the study Sepsis has well-documented inflammatory effects on cardiovascular and blood cells. This study is designed to investigate potential anti-inflammatory effects of metformin on cardiac and blood cells 12 and 24 h following cecal ligation and puncture (CLP)-induced sepsis. Methods For the purpose of this study, 36 male Wistar rats were divided into six groups: two groups underwent CLP, two groups underwent CLP and received metformin, and two groups only received sham operations. 12 h later, 18 rats (half of rats in each of the three aforementioned groups) were sacrificed and cardiac and blood cells were harvested. Subsequently, 12 h later, the rest of the rats were euthanatized. In all harvested blood and cardiac cells, oxidative stress indicators, antioxidant properties, count of blood cells, neutrophil infiltration, percentage of weight loss and pathological assessment were conducted. Results In our experiment, metformin elevated antioxidant levels, improved function of blood cells and percentage of weight loss. Moreover, in the groups which received metformin, oxidative stress and neutrophil infiltration markers were decreased significantly. Moreover, pathological investigations of cardiac cell injury were reduced in the metformin group. Conclusions Our findings suggest that in CLP induced sepsis model, metformin can improve the function of blood and cardiac cells through alleviating inflammation, improvement of anti-inflammation properties, and enhancement of blood profile, and all these effects are more pronounced after 24 h in comparison with 12 h after induction of sepsis.



2012 ◽  
Vol 113 (2) ◽  
pp. 519-528 ◽  
Author(s):  
Zhaohui Gao ◽  
Marsha Novick ◽  
Matthew D. Muller ◽  
Ronald J. Williams ◽  
Samson Spilk ◽  
...  


2011 ◽  
Vol 7 (3) ◽  
pp. 219-227 ◽  
Author(s):  
Francesco Angelico ◽  
Lorenzo Loffredo ◽  
Pasquale Pignatelli ◽  
Teresa Augelletti ◽  
Roberto Carnevale ◽  
...  


2005 ◽  
Vol 90 (5) ◽  
pp. 2653-2658 ◽  
Author(s):  
Angelika Mohn ◽  
Mariangela Catino ◽  
Rita Capanna ◽  
Cosimo Giannini ◽  
Maria Marcovecchio ◽  
...  


Life Sciences ◽  
2021 ◽  
pp. 120019
Author(s):  
V. Nagarjuna Reddy ◽  
Tan Pei Yin ◽  
Nelli Giribabu ◽  
Visweswara Rao Pasupuleti ◽  
Shaik Nyamathulla ◽  
...  


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jonas Neuser ◽  
Daniela Fraccarollo ◽  
Jan P Tuckermann ◽  
Paolo Galuppo ◽  
Johann Bauersachs

Background: Glucocorticoid administration impairs ischemic wound healing by inhibiting inflammation and angiogenesis via a glucocorticoid receptor (GR)-mediated transcriptional response. However, there are also apparently contradictory reports claiming protective effects of glucorticoid administration after myocardial infarction (MI). We investigated the role of the GR in myeloid cells for infarct wound healing, using GR deficient mice (GRLysMCre). Methods and Results: MI was induced by permanent left coronary artery ligation in GRflox (wild-type [WT] controls) and GRLysMCre mice. The 7-day mortality was significantly lower in WT compared with GRLysMCre mice. At 7 days post MI, GRLysMCre mice exhibited significantly enhanced thinning and dilatation of the infarcted wall, LV chamber enlargement and functional deterioration. This was associated with altered granulation tissue formation and impaired neoangiogenesis at the site of ischemic injury. Multicolor flow cytometric analysis and immunohistochemical studies revealed at the 2nd day post infarction less infiltrating mononuclear cells [CD11bhigh and (CD49b, NK1.1, B220, CD90, Ly6G)low] in the healing myocardium of GRLysMCre mice. Mononuclear cells were identified as monocytes (F4/80, I-Ab, CD11c)low and as macrophages/dendritic cells (F4/80, I-Ab, CD11c)high. Monocytes lacking GR, isolated from peripheral blood and spleen by magnetic-activated cell sorting 1 day after MI, displayed reduced migration capacity and increased superoxide anion production in mitochondria, which was detected by HPLC-electrochemical analysis of Mito-2-hydroxy-E+. Moreover, at day 2 and 3 we found enhanced cellular and mitochondrial oxidative stress in the healing myocardium of GRLysMCre mice. Conclusions: Myeloid-specific deletion of the GR increasing mitochondrial oxidative stress alters wound healing and promotes infarct expansion. Our results suggest that the GR in myeloid cells play a crucial role during cardiac repair after myocardial infarction.





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