Sok Kuan Wong

Dr. Sok Kuan Wong

Universiti Kebangsaan Malaysia (UKM)
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Academic Career Length

12Years (2015-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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4 October 2016 in Nutrition & Metabolism
Verified
Journal Article
Open access
PDF file
SWSok Kuan Wong
Sok Kuan Wong
Kok Yong ChinKok Yong Chin
Kok Yong Chin
FSFarihah Hj Suhaimi
Farihah Hj Suhaimi
FAFairus Ahmad
Fairus Ahmad
ISIma Soelaiman
Ima Soelaiman
Metabolic syndrome (MetS) consists of several medical conditions that collectively predict the risk for cardiovascular disease better than the sum of individual conditions. The risk of developing MetS in human depends on synergy of both genetic and environmental factors. Being a multifactorial condition with alarming rate of prevalence nowadays, establishment of appropriate experimental animal models mimicking the disease state in humans is crucial in order to solve the difficulties in evaluating the pathophysiology of MetS in human. This review aims to summarize the underlying mechanisms involved in the pathophysiology of dietary, genetic, and pharmacological models of MetS. Furthermore, we will discuss the usefulness, suitability, pros and cons of these animal models. Even though numerous animal models of MetS have been established, further investigations on the invention of new animal model and clarification of plausible mechanisms are still necessary to confer a better understanding to researchers on the selection of animal models for their studies.
21 June 2018 in The Aging Male
Verified
Journal Article
Closed access
NMNur-Vaizura Mohamad
Nur-Vaizura Mohamad
SWSok Kuan Wong
Sok Kuan Wong
WHWan Nuraini Wan Hasan
Wan Nuraini Wan Hasan
JJJames Jam Jolly
James Jam Jolly
MNMohd Fozi Nur-Farhana
Mohd Fozi Nur-Farhana
Kok Yong ChinKok Yong Chin
Kok Yong Chin
Testosterone is the predominant gonadal androgen in men. Low testosterone levels are found to be associated with an increased in metabolic risk and systematic inflammation. Since adipose tissue is a source of inflammatory cytokines, testosterone may regulate inflammation by acting on adipose tissue. This review aimed to explore the role of testosterone in inflammation and its mechanism of action. Both animal studies and human studies showed that (1) testosterone deficiency was associated with an increase in pro-inflammatory cytokines; (2) testosterone substitution reduced pro-inflammatory cytokines. The suppression of inflammation by testosterone were observed in patients with coronary artery disease, prostate cancer and diabetes mellitus through the increase in anti-inflammatory cytokines (IL-10) and the decrease in pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). Despite these, some studies also reported a non-significant relationship. In conclusion, testosterone may possess anti-inflammatory properties but its magnitude is debatable. More evidence is needed to validate the use of testosterone as a marker and in the management of chronic inflammatory diseases.
25 October 2018 in International Journal of Environmental Research and Public Health
Verified
Journal Article
Open access
PDF file
NINurul 'Izzah Ibrahim
Nurul 'Izzah Ibrahim
SWSok Kuan Wong
Sok Kuan Wong
IMIsa Naina Mohamed
Isa Naina Mohamed
NMNorazlina Mohamed
Norazlina Mohamed
Kok Yong ChinKok Yong Chin
Kok Yong Chin
ASAhmad Nazrun Shuid
Ahmad Nazrun Shuid
Wound healing is a complex process of recovering the forms and functions of injured tissues. The process is tightly regulated by multiple growth factors and cytokines released at the wound site. Any alterations that disrupt the healing processes would worsen the tissue damage and prolong repair process. Various conditions may contribute to impaired wound healing, including infections, underlying diseases and medications. Numerous studies on the potential of natural products with anti-inflammatory, antioxidant, antibacterial and pro-collagen synthesis properties as wound healing agents have been performed. Their medicinal properties can be contributed by the content of bioactive phytochemical constituents such as alkaloids, essential oils, flavonoids, tannins, saponins, and phenolic compounds in the natural products. This review highlights the in vitro, in vivo and clinical studies on wound healing promotions by the selected natural products and the mechanisms involved.
3 September 2020 in International Journal of Molecular Sciences
Verified
Journal Article
Open access
PDF file
SWSok Kuan Wong
Sok Kuan Wong
Kok Yong ChinKok Yong Chin
Kok Yong Chin
ISIma Soelaiman
Ima Soelaiman
Quercetin is a flavonoid abundantly found in fruits and vegetables. It possesses a wide spectrum of biological activities, thus suggesting a role in disease prevention and health promotion. The present review aimed to uncover the bone-sparing effects of quercetin and its mechanism of action. Animal studies have found that the action of quercetin on bone is largely protective, with a small number of studies reporting negative outcomes. Quercetin was shown to inhibit RANKL-mediated osteoclastogenesis, osteoblast apoptosis, oxidative stress and inflammatory response while promoting osteogenesis, angiogenesis, antioxidant expression, adipocyte apoptosis and osteoclast apoptosis. The possible underlying mechanisms involved are regulation of Wnt, NF-κB, Nrf2, SMAD-dependent, and intrinsic and extrinsic apoptotic pathways. On the other hand, quercetin was shown to exert complex and competing actions on the MAPK signalling pathway to orchestrate bone metabolism, resulting in both stimulatory and inhibitory effects on bone in parallel. The overall interaction is believed to result in a positive effect on bone. Considering the important contributions of quercetin in regulating bone homeostasis, it may be considered an economical and promising agent for improving bone health. The documented preclinical findings await further validation from human clinical trials.
27 May 2019 in International Journal of Molecular Sciences
Verified
Journal Article
Open access
PDF file
SWSok Kuan Wong
Sok Kuan Wong
NMNur-Vaizura Mohamad
Nur-Vaizura Mohamad
TRTijjani Giaze Rabiu
Tijjani Giaze Rabiu
Kok Yong ChinKok Yong Chin
Kok Yong Chin
NMNorazlina Mohamed
Norazlina Mohamed
ISIma Soelaiman
Ima Soelaiman
Patients with advanced prostate cancer often develop bone metastases, leading to bone pain, skeletal fracture, and increased mortality. Bone provides a hospitable microenvironment to tumor cells. The disease manifestation is driven by the interaction between invading tumor cells, bone-forming osteoblasts, and bone-resorbing osteoclasts. The increased level of osteoclast-activating factor (parathyroid hormone-related peptide, PTHrP) is believed to induce bone resorption by upregulating receptor activator of nuclear factor-kappa B ligand (RANKL) and the release of various growth factors into the bone microenvironment to enhance cancer cell growth. However, the underlying molecular mechanisms remain poorly understood. This review outlines the possible molecular mechanisms involved in governing bone metastases driven by prostate cancer, which further provide the basis in searching for new molecular targets for the development of potential therapy.
7 June 2016 in Nutrients
Verified
Journal Article
Open access
PDF file
SWSok Kuan Wong
Sok Kuan Wong
Kok Yong ChinKok Yong Chin
Kok Yong Chin
FSFarihah Hj Suhaimi
Farihah Hj Suhaimi
FAFairus Ahmad
Fairus Ahmad
ISIma Soelaiman
Ima Soelaiman
Metabolic syndrome (MetS) and osteoporosis are two major healthcare problems worldwide. Metabolic syndrome is a constellation of medical conditions consisting of central obesity, hyperglycemia, hypertension, and dyslipidemia, in which each acts on bone tissue in different ways. The growing prevalence of MetS and osteoporosis in the population along with the controversial findings on the relationship between both conditions suggest the importance for further investigation and discussion on this topic. This review aims to assess the available evidence on the effects of each component of MetS on bone metabolism from the conventional to the contemporary. Previous studies suggested that the two conditions shared some common underlying pathways, which include regulation of calcium homeostasis, receptor activator of NF-κB ligand (RANKL)/receptor activator of the NF-κB (RANK)/osteoprotegerin (OPG) and Wnt-β-catenin signaling pathways. In conclusion, we suggest that MetS may have a potential role in developing osteoporosis and more studies are necessary to further prove this hypothesis.