Pharmacological evaluation of aqueous extract of syzigium cumini for its antihyperglycemic and antidyslipidemic properties in diabetic rats fed a high cholesterol diet—Role of PPARγ and PPARα

Sharma, Shiveta; Pathak, Sachchidanand; Gupta, Gaurav; Sharma, Satish Kumar; Singh, Lalit; Sharma, Rakesh; Mishra, Anurag; Dua, Kamal

doi:10.1016/j.biopha.2017.02.048

Cited by 63 publications

(30 citation statements)

References 27 publications

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“…However, it is undoubted that several still unexplored natural sources of potential PPAR α modulators are available. Thus, the list reported in Table 175, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112 is should encourage natural product chemists to make efforts aimed at the detailed characterization of the active principle(s) responsible for the action of these extract.…”

Section: Natural Products Modulating Pparαmentioning

confidence: 99%

The potential of natural products for targeting PPAR α

Rigano

Sirignano

Taglialatela‐Scafati

2017

Acta Pharmaceutica Sinica B

128

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Peroxisome proliferator activated receptors (PPARs) α, -γ and -β/δ are ligand-activated transcription factors and members of the superfamily of nuclear hormone receptor. These receptors play key roles in maintaining glucose and lipid homeostasis by modulating gene expression. PPARs constitute a recognized druggable target and indeed several classes of drugs used in the treatment of metabolic disease symptoms, such as dyslipidemia (fibrates, e.g. fenofibrate and gemfibrozil) and diabetes (thiazolidinediones, e.g. rosiglitazone and pioglitazone) are ligands for the various PPAR isoforms. More precisely, antidiabetic thiazolidinediones act on PPARγ, while PPARα is the main molecular target of antidyslipidemic fibrates. Over the past few years, our understanding of the mechanism underlying the PPAR modulation of gene expression has greatly increased. This review presents a survey on terrestrial and marine natural products modulating the PPARα system with the objective of highlighting how the incredible chemodiversity of natural products can provide innovative leads for this “hot” target.

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Section: Natural Products Modulating Pparαmentioning

confidence: 99%

The potential of natural products for targeting PPAR α

Rigano

Sirignano

Taglialatela‐Scafati

2017

Acta Pharmaceutica Sinica B

128

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“…Met and Lut had a synergistic defensive impact if there could be an occurrence of CCl 4 ‐prompted serum and biochemical adjustments in the hepatic tissues. The defensive impact, according to the present investigation results, may be because of ROS scavenging and restraint of LPO, which are direct methods . It might likewise be because of improved antioxidative enzyme action, which is viewed as the indirect method.…”

Section: Discussionmentioning

confidence: 49%

Combination of metformin and luteolin synergistically protects carbon tetrachloride‐induced hepatotoxicity: Mechanism involves antioxidant, anti‐inflammatory, antiapoptotic, and Nrf2/HO‐1 signaling pathway

Yang¹,

Yang²,

Jiangmei³

2019

BioFactors

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Liver diseases are one of the fatal disorders due to the vital role of the liver. Carbon tetrachloride (CCl4) is the most perceived chemical substance utilized in developing models of hepatic damage. Metformin (Met) is a potent antidiabetic and redox modulatory agent that has shown anticancer and protective effects on various organs. Therefore, addition of therapy with natural antioxidative agents or herbal extracts shows defensive impacts against different injuries inside the body. Luteolin (Lut) can be found in several customary Chinese remedies. It has been reported for various pharmacological actions such as antitumor, antioxidative, and anti‐inflammatory impacts. Here, the liver injury rat model was established using CCl4 (1.00 mL/kg body weight) in vivo. The protective roles of Met and Lut separately or in combination were observed in hepatotoxicity induced by CCl4. The result was shown that both Met and Lut, while individually used, were normally active in diminishing CCl4‐caused hepatotoxicity. The combination of two drugs performed synergistically to improve liver damage caused by CCl4, as shown by the considerably improved liver dysfunction. Met and Lut showed highly antioxidative effects on CCl4‐treated rats moderately by increasing the activities and expression of the antioxidant enzymes. Along with this, a combination of Met and Lut significantly suppressed inflammatory responses, which is evidenced by the reduced level of inflammatory cytokines together with interleukin 1 beta (IL‐1β), tumor necrosis factor alpha (TNF‐α), and interleukin 6 (IL‐6). Additionally, CCl4‐agitated apoptosis was intensely reduced by Met and Lut through reducing cleaved caspase‐3 and Bax (pro‐apoptotic factor) while increasing Bcl‐2 (antiapoptotic factor) signaling pathways. Cotreatments of Met and Lut upregulated nuclear factor erythroid 2‐related factor 2 (NRF2) and heme oxygenase‐1 (HO‐1) expression in the CCl4‐intoxicated rat's liver. The above result recommended that combination of Met and Lut may have a substantial potential and synergizing impact against CCl4‐induced hepatotoxicity.

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“…Once the compensatory mechanism fails to maintain the preserved cardiac output via enhancing the consequence of down regulation of the performance of β‐ARs. Thus, another event of activity in HF reduced ejection fraction (HFrEF) taken place via activation of the renin‐angiotensin‐aldosterone system (RAAS; Sharma et al, ). The RAAS is a central feature in the pathophysiology of HF (Sayer & Bhat, ).…”

Section: Pathophysiology Of Hf and Associated Cardiac Hypertrophymentioning

confidence: 99%

Molecular signaling of G‐protein‐coupled receptor in chronic heart failure and associated complications

Altamish

Samuel

Dahiya

et al. 2019

Drug Development Research

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The well‐known condition of heart failure is a clinical syndrome that results when the myocardium's ability to pump enough blood to meet the body's metabolic needs is impaired. Most of the cardiac activity is maintained by adrenoceptors, are categorized into two main α and β and three distinct subtypes of β receptor: β1‐, β2‐, and β3‐adrenoceptors. The β adrenoreceptor is the main regulatory macro proteins, predominantly available on heart and responsible for down regulatory cardiac signaling. Moreover, the pathological involvement of Angiotensin‐converting enzyme 1 (ACE1)/angiotensin II (Ang II)/angiotensin II type 1 (AT1) axis and beneficial ACE2/Ang (1‐7)/Mas receptor axis also shows protective role via Gi βγ, during heart failure these receptors get desensitized or internalized due to increase in the activity of G‐protein‐coupled receptor kinase 2 (GRK2) and GRK5, responsible for phosphorylation of G‐protein‐mediated down regulatory signaling. Here, we investigate the various clinical and preclinical data that exhibit the molecular mechanism of upset level of GRK change the cardiac activity during failing heart.

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Pharmacological evaluation of aqueous extract of syzigium cumini for its antihyperglycemic and antidyslipidemic properties in diabetic rats fed a high cholesterol diet—Role of PPARγ and PPARα

Cited by 63 publications

References 27 publications

The potential of natural products for targeting PPAR α

The potential of natural products for targeting PPAR α

Combination of metformin and luteolin synergistically protects carbon tetrachloride‐induced hepatotoxicity: Mechanism involves antioxidant, anti‐inflammatory, antiapoptotic, and Nrf2/HO‐1 signaling pathway

Molecular signaling of G‐protein‐coupled receptor in chronic heart failure and associated complications

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