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  1. Sukalingam K, Ganesan K, Das S, Thent ZC
    Clin Ter, 2015;166(3):131-9.
    PMID: 26152621 DOI: 10.7417/CT.2015.1843
    Soy protein (SP) is a protein derived from soybean meal. SP is obtained from the removal of the outer shell of soybean and the fatty acid. The dietary supplementation of SP was was reported to have positive effects on human health. Therefore, the attention towards SP is increasing among the consumers, industrialist and researchers. However, the side effects and toxicity related to SP was not summarized, to date. This review summarized the toxic effects such as hormonal disturbances, carcinogenic and organotoxicity of SP based on the clinical and experimental studies. The review mainly focused on the effect of soy isoflavone-genistein on various organs. The main aim of the present review is to increase the public awareness on the harmful effect of SP on the various health aspects and draw the attention of the health care personnel and researchers.
  2. Sukalingam K, Ganesan K, Xu B
    Antioxidants (Basel), 2018 Jun 22;7(7).
    PMID: 29932107 DOI: 10.3390/antiox7070078
    The present study aims to examine the protective effect of Justicia tranquebariesis on thioacetamide (TAA)-induced oxidative stress and hepatic fibrosis. Male Wister albino rats (150⁻200 g) were divided into five groups. Group 1 was normal control. Group 2 was J. tranquebariensis (400 mg/kg bw/p.o.)-treated control. Group 3 was TAA (100 mg/kg bw/s.c.)-treated control. Groups 4 and 5 were orally administered with the leaf extract of J. tranquebariensis (400 mg/kg bw) and silymarin (50 mg/kg bw) daily for 10 days with a subsequent administration of a single dose of TAA (100 mg/kg/s.c.). Blood and livers were collected and assayed for various antioxidant enzymes (SOD, CAT, GPx, GST, GSH, and GR). Treatment with J. tranquebariensis significantly reduced liver TBARS and enhanced the activities of antioxidant enzymes in TAA-induced fibrosis rats. Concurrently, pretreatment with J. tranquebariensis significantly reduced the elevated liver markers (AST, ALT, ALP, GGT, and TB) in the blood. In addition, J. tranquebariensis- and silymarin- administered rats demonstrated the restoration of normal liver histology and reduction in fibronectin and collagen deposition. Based on these findings, J. tranquebariensis has potent liver protective functions and can alleviate thioacetamide-induced oxidative stress, hepatic fibrosis and possible engross mechanisms connected to antioxidant potential.
  3. Mohd Ramli ES, Sukalingam K, Kamaruzzaman MA, Soelaiman IN, Pang KL, Chin KY
    Diabetes Metab Syndr Obes, 2021;14:241-256.
    PMID: 33500644 DOI: 10.2147/DMSO.S291828
    Metabolic syndrome (MetS) refers to the simultaneous presence of hypertension, hyperglycemia, dyslipidemia and/or visceral obesity, which predisposes a person to cardiovascular diseases and diabetes. Evidence suggesting the presence of direct and indirect associations between MetS and osteoporosis is growing. Many studies have reported the beneficial effects of polyphenols in alleviating MetS in in vivo and in vitro models through their antioxidant and anti-inflammation actions. This review aims to summarize the effects of honey (based on unifloral and multi-floral nectar sources) on bone metabolism and each component of MetS. A literature search was performed using the PubMed and Scopus databases using specific search strings. Original studies related to components of MetS and bone, and the effects of honey on components of MetS and bone were included. Honey polyphenols could act synergistically in alleviating MetS by preventing oxidative damage and inflammation. Honey intake is shown to reduce blood glucose levels and prevent excessive weight gain. It also improves lipid metabolism by reducing total cholesterol, triglycerides and low-density lipoprotein, as well as increasing high-density lipoprotein. Honey can prevent bone loss by reducing the adverse effects of MetS on bone homeostasis, apart from its direct action on the skeletal system. In conclusion, honey supplementation could be integrated into the management of MetS and MetS-induced bone loss as a preventive and adjunct therapeutic agent.
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