Ipomea aquatica, locally known as water spinach, is one of the most common vegetable consumed by
Malaysian. Based on previous studies, crude extract and phenolic compounds of I. aquatica exhibited
several biological activities including antioxidant, anti-microbial and anti-proliferative. The presence
of phenolic compounds in I. aquatica may contributed to their ability to inhibit enzymes, chelate
metals and scavenge free radicals. Currently, no study reported on anti-inflammatory activity of I.
aquatica with respect to lipoxygenase, hyaluronidase and xanthine oxidase enzymes. The present
study aims to enhance current knowledge on biological properties of I. aquatica crude extract
particularly on anti-inflammatory activity. Three enzymes that involve in inflammatory pathway were
selected in this study including lipoxygenase, hyaluronidase and xanthine oxidase. I. aquatica was
extracted in methanol and tested for lipoxygenase, hyaluronidase and xanthine oxidase at different
concentrations using direct enzyme inhibition assay. Lipoxygenase, hyaluronidase and xanthine
oxidase inhibitory activities of the methanol crude extract increased with increasing
concentration. Highest inhibition activity against lipoxygenase, hyaluronidase and xanthine oxidase
were observed at a concentration of 1000 µg/ml with inhibition of 87.18%, 95.36% and 78.38%,
respectively. Our finding in this study indicates potential anti-inflammatory activity of I. aquatica
crude extract through inhibition of lipoxygenase, hyaluronidase and xanthine oxidase.
Insulin resistance is characterized by hyperglycaemia, dyslipidaemia and oxidative stress prior to the development of type 2 diabetes mellitus. To date, a number of mechanisms have been proposed to link these syndromes together, but it remains unclear what the unifying condition that triggered these events in the progression of this metabolic disease. There have been a steady accumulation of data in numerous experimental studies showing the strong correlations between mitochondrial dysfunction, oxidative stress and insulin resistance. In addition, a growing number of studies suggest that the raised plasma free fatty acid level induced insulin resistance with the significant alteration of oxidative metabolism in various target tissues such as skeletal muscle, liver and adipose tissue. In this review, we herein propose the idea of long chain fatty acid-induced mitochondrial dysfunctions as one of the key events in the pathophysiological development of insulin resistance and type 2 diabetes. The accumulation of reactive oxygen species, lipotoxicity, inflammation-induced endoplasmic reticulum stress and alterations of mitochondrial gene subset expressions are the most detrimental that lead to the developments of aberrant intracellular insulin signalling activity in a number of peripheral tissues, thereby leading to insulin resistance and type 2 diabetes.