Anti-inflammatory property of Kalpaamruthaa on myocardium in type 2 diabetes mellitus induced cardiovascular complication

2012 ◽  
Vol 35 (1) ◽  
pp. 119-125 ◽  
Author(s):  
Latha Raja ◽  
Shanthi Palanivelu ◽  
Sachdanandam Panchanatham
2015 ◽  
Vol 6 (9) ◽  
pp. 3065-3071 ◽  
Author(s):  
Wenbin Yin ◽  
Baoying Li ◽  
Xiaoli Li ◽  
Fei Yu ◽  
Qian Cai ◽  
...  

The prevalence of type 2 diabetes mellitus (T2DM) has increased considerably in recent years, highlighting the importance of developing new therapeutic strategies.


Author(s):  
Saffiya Banu. A ◽  
Sheila John ◽  
Sarah Jane Monica ◽  
Saraswathi. K ◽  
Arumugam. P

Recent research studies indicate the role of functional foods in preventing the development of complications associated with type 2 diabetes mellitus. Chia seeds are an excellent source of dietary fibre, essential fatty acids, micronutrients and non-nutritive components. The objective of the study was to evaluate the antioxidant, antibacterial, antidiabetic and anti-inflammatory potential of chia seeds. TPC and TFC were estimated using Folin-Ciocalteu Reagent and Alumininum Chloride method. The antioxidant activity was determined using DPPH● radical, ABTS●+ radical, Superoxide (O2-) radical, Fe3+ reducing and phosphomolybdenum reduction assay. Agar well diffusion method was used to determine the antibacterial activity against Escherichia coli, Proteus vulgaris, Shigella flexneri, Micrococcus luteus, Bacillus subtilis and Staphylococcus aureus. Antidiabetic and anti-inflammatory activities were evaluated using alpha amylase inhibition assay and heat induced haemolysis method. Volatile functional compounds were identified using Gas chromatography mass spectrometry. Upon quantification, TPC and TFC were found to be 850.67±14.14µg/mg GAE and 171.21±12.86µg/mg QE. Free radical scavenging activity of chia seeds was ranked in the order of DPPH● radical >ABTS●+ radical > Superoxide (O2-) radical. The capability of chia seeds to function as electron donors was evident through its strong reducing power. With regard to antibacterial activity, maximum inhibition was observed for Staphylococcus aureus, with a zone of inhibition of 31mm at 500µg/mL. Results of antidiabetic assay highlighted the alpha amylase inhibitory action of chia seeds with an IC50 value of 121.46µg/mL. The anti-inflammatory activity of chia seeds increased linearly in a dose dependent manner. GC-MS analysis showed the presence of functionally active compounds such as coumarine, napthoquinone, phytol, fatty acids, flavone and flavone derivatives. Findings of the study highlight that chia seeds have several essential therapeutic properties. Furthermore, clinical studies are required to validate the role of chia seeds in preventing the development of complications associated with type 2 diabetes mellitus.


2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Rafael Nepomuceno ◽  
Bárbara Scoralick Villela ◽  
Sâmia Cruz Tfaile Corbi ◽  
Alliny De Souza Bastos ◽  
Raquel Alves Dos Santos ◽  
...  

A high percentage of type 2 diabetes mellitus (T2D) patients are also affected by dyslipidemia and chronic periodontitis (CP), but no studies have determined the gene expression in patients that are simultaneously affected by all three diseases. We investigated the systemic expression of immune-related genes in T2D, dyslipidemia, and CP patients. One hundred and fifty patients were separated into five groups containing 30 individuals each: (G1) poorly controlled T2D with dyslipidemia and CP; (G2) well-controlled T2D with dyslipidemia and CP; (G3) normoglycemic individuals with dyslipidemia and CP; (G4) healthy individuals with CP; (G5) systemic and periodontally healthy individuals. Blood analyses of lipid and glycemic profiles were carried out. The expression of genes, includingIL10, JAK1, STAT3, SOCS3, IP10, ICAM1, IFNA, IFNG, STAT1,andIRF1,was investigated by RT-qPCR. Patients with dyslipidemia demonstrated statistically higher expression of theIL10andIFNAgenes, whileIFNG, IP10, IRF1, JAK1,andSTAT3were lower in comparison with nondyslipidemic patients. Anti-inflammatory genes, such asIL10, positively correlated with parameters of glucose, lipid, and periodontal profiles, while proinflammatory genes, such asIFNG, were negatively correlated with these parameters. We conclude that dyslipidemia appears to be the primary disease that is associated with gene expression of immune-related genes, while parameters of T2D and CP were correlated with the expression of these important immune genes.


2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Li Zheng ◽  
Wei Zhang ◽  
Aimei Li ◽  
Yan Liu ◽  
Bin Yi ◽  
...  

Objective. Inflammation plays a major role in albuminuria in type 2 diabetes mellitus (T2DM). Our previous studies have shown that the expression of vitamin D receptor (VDR) is downregulated in T2DM which is closely associated with the severity of albuminuria. In this study, we investigated the expression of anti-inflammatory cytokine protein tyrosine phosphatase nonreceptor type 2 (PTPN2) in T2DM and explored its relationship to albuminuria and VDR. Methods. 101 T2DM patients were divided into three groups based on urinary albumin-to-creatinine ratio (uACR): normal albuminuria (uACR < 30 mg/g, n=29), microalbuminuria (30 mg/g ≤ uACR < 300 mg/g, n=34), and macroalbuminuria (uACR ≥ 300 mg/g, n=38). Thirty healthy individuals were included as controls. Serum was analyzed for PTPN2 and IL-6 expression, and peripheral blood mononuclear cells (PBMCs) were analyzed for PTPN2 and VDR expression. THP-1 cells were incubated with high glucose and further treated with or without paricalcitol, a vitamin D analog. The levels of PTPN2, VDR, IL-6, TNFα, and MCP-1 were analyzed. In addition, anti-inflammatory activities of PTPN2 were further explored in THP-1 cells stimulated with high glucose after PTPN2 silencing or overexpression. Results. PTPN2 expression was downregulated in T2DM with the lowest level observed in macroalbuminuria patients. PTPN2 level positively correlated with VDR but negatively correlated with uACR and IL-6. When stimulated with high glucose, there was an increase in inflammatory factors and a decrease in PTPN2 expression. Treatment with paricalcitol reversed these effects. However, paricalcitol failed to exert anti-inflammatory effects in the setting of PTPN2 knockdown. Thus, low levels of PTPN2 aggravated glucose-stimulated inflammation, while high levels of PTPN2 reduced it. Conclusion. PTPN2, an anti-inflammatory factor regulated by VDR, was reduced in T2DM CKD stages 1-2. Taken together, our results suggest that therapeutic strategies that enhance PTPN2 may be beneficial for controlling inflammation in T2DM.


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