Displaying publications 121 - 126 of 126 in total

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  1. Kassim M, Achoui M, Mansor M, Yusoff KM
    Fitoterapia, 2010 Dec;81(8):1196-201.
    PMID: 20708657 DOI: 10.1016/j.fitote.2010.07.024
    We investigated the effects of honey and its methanol and ethyl acetate extracts on inflammation in animal models. Rats' paws were induced with carrageenan in the non-immune inflammatory and nociceptive model, and lipopolysaccharide (LPS) in the immune inflammatory model. Honey and its extracts were able to inhibit edema and pain in inflammatory tissues as well as showing potent inhibitory activities against NO and PGE(2) in both models. The decrease in edema and pain correlates with the inhibition of NO and PGE(2). Phenolic compounds have been implicated in the inhibitory activities. Honey is potentially useful in the treatment of inflammatory conditions.
    Matched MeSH terms: Inflammation/drug therapy*
  2. Muniandy S, Qvist R, Yan GO, Bee CJ, Chu YK, Rayappan AV
    J. Med. Invest., 2009 Feb;56(1-2):6-10.
    PMID: 19262007
    Hyperglycemia and insulin resistance are common in many critically ill patients. Hyperglycemia increases the production of reactive oxygen species in cells, stimulates the production of the potent proinflammatory cytokines IL-8 and TNF-alpha, and enhances the expression of haem oxygenase-1, an inducible stress protein. It has been shown that administration of insulin and the semi-essential amino acid glutamine have been beneficial to the septic patient. The aim of our study is to test whether these two molecules, glutamine and insulin used in combination attenuate the proinflammatory responses in endothelial cells which have been triggered by hyperglycaemia. Our results demonstrate that a combination of insulin and glutamine are significantly more effective in reducing the expression of IL-8, TNF-alpha and HO-1 than insulin or glutamine alone.
    Matched MeSH terms: Inflammation/drug therapy
  3. Siti HN, Kamisah Y, Kamsiah J
    Vascul. Pharmacol., 2015 Aug;71:40-56.
    PMID: 25869516 DOI: 10.1016/j.vph.2015.03.005
    The concept of mild chronic vascular inflammation as part of the pathophysiology of cardiovascular disease, most importantly hypertension and atherosclerosis, has been well accepted. Indeed there are links between vascular inflammation, endothelial dysfunction and oxidative stress. However, there are still gaps in our understanding regarding this matter that might be the cause behind disappointing results of antioxidant therapy for cardiovascular risk factors in large-scale long-term randomised controlled trials. Apart from the limitations of our knowledge, limitations in methodology and assessment of the body's endogenous and exogenous oxidant-antioxidant status are a serious handicap. The pleiotropic effects of antioxidant and anti-inflammation that are shown by some well-established antihypertensive agents and statins partly support the idea of using antioxidants in vascular diseases as still relevant. This review aims to provide an overview of the links between oxidative stress, vascular inflammation, endothelial dysfunction and cardiovascular risk factors, importantly focusing on blood pressure regulation and atherosclerosis. In view of the potential benefits of antioxidants, this review will also examine the proposed role of vitamin C, vitamin E and polyphenols in cardiovascular diseases as well as the success or failure of antioxidant therapy for cardiovascular diseases in clinical trials.
    Matched MeSH terms: Inflammation/drug therapy
  4. Sharma JN
    Gen. Pharmacol., 1993 Mar;24(2):267-74.
    PMID: 8387049
    1. Bradykinin and related kinins may act on four types of receptors designated as B1, B2, B3 and B4. It seems that the B2 receptors are most commonly found in various vascular and non-vascular smooth muscles, whereas B1 receptors are formed in vitro during trauma, and injury, and are found in bone tissues. 2. These BK receptors are involved in the regulations of various physiological and pathological processes. 3. The mode of kinin actions are based upon the interactions between the kinin and their specific receptors, which can lead to activation of several second-messenger systems. 4. Recently, numerous BK receptors antagonists have been synthesized with prime aim to treat diseases caused by excessive kinin production. 5. These diseases are RA, inflammatory diseases of the bowel, asthma, rhinitis and sore throat, allergic reactions, pain, inflammatory skin disorders, endotoxin and anaphylactic shock and coronary heart diseases. 6. On the other hand, BK receptor antagonists could be contraindicated in hypertension, since these drugs may antagonize the antihypertensive therapy and/or may trigger the hypertensive crisis. 7. It is worth suggesting that the BK receptor agonists might be useful antihypertensive drugs.
    Matched MeSH terms: Inflammation/drug therapy*
  5. Sadikan MZ, Abdul Nasir NA, Bakar NS, Iezhitsa I, Agarwal R
    BMC Complement Med Ther, 2023 Jun 02;23(1):179.
    PMID: 37268913 DOI: 10.1186/s12906-023-04005-9
    BACKGROUND: Diabetic retinopathy (DR) is the second commonest microvascular complication of diabetes mellitus. It is characterized by chronic inflammation and angiogenesis. Palm oil-derived tocotrienol-rich fraction (TRF), a substance with anti-inflammatory and anti-angiogenic properties, may provide protection against DR development. Therefore, in this study, we investigated the effect of TRF on retinal vascular and morphological changes in diabetic rats. The effects of TRF on the retinal expression of inflammatory and angiogenic markers were also studied in the streptozotocin (STZ)-induced diabetic rats.

    METHODS: Male Sprague Dawley rats weighing 200-250 g were grouped into normal rats (N) and diabetic rats. Diabetes was induced by intraperitoneal injection of streptozotocin (55 mg/kg body weight) whereas N similarly received citrate buffer. STZ-injected rats with blood glucose of more than 20 mmol/L were considered diabetic and were divided into vehicle-treated (DV) and TRF-treated (DT) groups. N and DV received vehicle, whereas DT received TRF (100 mg/kg body weight) via oral gavage once daily for 12 weeks. Fundus images were captured at week 0 (baseline), week 6 and week 12 post-STZ induction to estimate vascular diameters. At the end of experimental period, rats were euthanized, and retinal tissues were collected for morphometric analysis and measurement of NFκB, phospho-NFκB (Ser536), HIF-1α using immunohistochemistry (IHC) and enzyme-linked immunosorbent assay (ELISA). Retinal inflammatory and angiogenic cytokines expression were measured by ELISA and real-time quantitative PCR.

    RESULTS: TRF preserved the retinal layer thickness (GCL, IPL, INL and OR; p 

    Matched MeSH terms: Inflammation/drug therapy
  6. Wong SK, Chin KY, Ima-Nirwana S
    Int J Med Sci, 2020;17(11):1625-1638.
    PMID: 32669965 DOI: 10.7150/ijms.47103
    Oxidative stress and inflammation are two interlinked events that exist simultaneously in metabolic syndrome (MetS) and its related complications. These pathophysiological processes can be easily triggered by each other. This review summarizes the current evidence from animal and human studies on the effects of vitamin C in managing MetS. In vivo studies showed promising effects of vitamin C, but most of the interventions used were in combination with other compounds. The direct effects of vitamin C remain to be elucidated. In humans, the current state of evidence revealed that lower vitamin C intake and circulating concentration were found in MetS subjects. A negative relationship was observed between vitamin C intake / concentration and the risk of MetS. Oral supplementation of vitamin C also improved MetS conditions. It has been postulated that the positive outcomes of vitamin C may be in part mediated through its anti-oxidative and anti-inflammatory properties. These observations suggest the importance of MetS patients to have an adequate intake of vitamin C through food, beverages or supplements in order to maintain its concentration in the systemic circulation and potentially reverse MetS.
    Matched MeSH terms: Inflammation/drug therapy
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