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Displaying publications 61 - 67 of 67 in total

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The current and future perspectives of zinc oxide nanoparticles in the treatment of diabetes mellitus

Tang KS

Life Sci, 2019 Dec 15;239:117011.
PMID: 31669241 DOI: 10.1016/j.lfs.2019.117011

Diabetes mellitus (DM) is a multifaceted and costly disease, which requires serious attention. Finding a cheaper anti-diabetic alternative that can act on multiple disease-related targets and pathways is the ultimate treatment goal for DM. Nanotechnology has offered some exciting possibilities in biomedical and drug delivery applications. Zinc oxide nanoparticles (ZnO-NPs), a novel agent to deliver zinc, have great implications in many disease therapies including DM. This review summarizes the pharmacological mechanisms by which ZnO-NPs alleviate DM and diabetic complications. Research implications and future perspectives were also discussed.
The potential role of nanoyttria in alleviating oxidative stress biomarkers: Implications for Alzheimer's disease therapy

Tang KS

Life Sci, 2020 Oct 15;259:118287.
PMID: 32814066 DOI: 10.1016/j.lfs.2020.118287

Alzheimer's disease (AD) is a fatal neurodegenerative disease that requires immediate attention. Oxidative stress that leads to the generation of reactive oxygen species is a contributing factor to the disease progression by promoting synthesis and deposition of amyloid-β, the main hallmark protein in AD. It has been previously demonstrated that nanoyttria possesses antioxidant properties and can alleviate cellular oxidative injury in various toxicity and disease models. This review proposed that nanoyttria could be used for the treatment of AD. In this paper, the evidence on the antioxidant potential of nanoyttria is presented and its prospects on AD therapy are discussed.
The prevention and treatment of hypoadiponectinemia-associated human diseases by up-regulation of plasma adiponectin

Hossain MM, Mukheem A, Kamarul T

Life Sci, 2015 Aug 15;135:55-67.
PMID: 25818192 DOI: 10.1016/j.lfs.2015.03.010

Hypoadiponectinemia is characterized by low plasma adiponectin levels that can be caused by genetic factors, such as single nucleotide polymorphisms (SNPs) and mutations in the adiponectin gene or by visceral fat deposition/obesity. Reports have suggested that hypoadiponectinemia is associated with dyslipidemia, hypertension, hyperuricemia, metabolic syndrome, atherosclerosis, type 2 diabetes mellitus and various cardiovascular diseases. Previous studies have highlighted several potential strategies to up-regulate adiponectin secretion and function, including visceral fat reduction through diet therapy and exercise, administration of exogenous adiponectin, treatment with peroxisome proliferator-activating receptor gamma (PPARγ) agonists (e.g., thiazolidinediones (TZDs)) and ligands (e.g., bezafibrate and fenofibrate) or the blocking of the renin-angiotensin system. Likewise, the up-regulation of the expression and stimulation of adiponectin receptors by using adiponectin receptor agonists would be an effective method to treat obesity-related conditions. Notably, adiponectin is an abundantly expressed bioactive protein that also exhibits a wide spectrum of biological properties, such as insulin-sensitizing, anti-diabetic, anti-inflammatory and anti-atherosclerotic activities. Although targeting adiponectin and its receptors has been useful for treating diabetes and other metabolic-related diseases in experimental studies, current drug development based on adiponectin/adiponectin receptors for clinical applications is scarce, and there is a lack of available clinical trial data. This comprehensive review discusses the strategies that are presently being pursued to harness the potential of adiponectin up-regulation. In addition, we examined the current status of drug development and its potential for clinical applications.
Fulltext The role of TNFR2+ Tregs in COVID-19: An overview and a potential therapeutic strategy

Ahmad S, Hatmal MM, Lambuk L, Al-Hatamleh MAI, Alshaer W, Mohamud R

Life Sci, 2021 Dec 01;286:120063.
PMID: 34673116 DOI: 10.1016/j.lfs.2021.120063

COVID-19 is a multi-faceted disease ranging from asymptomatic to severely ill condition that primarily affects the lungs and could advance to other organs as well. It's causing factor, SARS-CoV-2 is recognized to develop robust cell-mediated immunity that responsible to either control or exaggerate the infection. As an important cell subset that control immune responses and are significantly dysregulated in COVID-19, Tregs is proposed to be considered for COVID-19 management. Among its hallmark, TNFR2 is recently recognized to play important role in the function and survival of Tregs. This review gathers available TNFR2 agonists to directly target Tregs as a potential approach to overcome immune dysregulation that affect the severity in COVID-19. Furthermore, this review performs a rigid body docking of TNF-TNFR2 interaction and such interaction with TNFR2 agonist to predict the optimal targeting approach.
The use of delta-tocotrienol and lovastatin for anti-osteoporotic therapy

Abdul-Majeed S, Mohamed N, Soelaiman IN

Life Sci, 2015 Mar 15;125:42-8.
PMID: 25534439 DOI: 10.1016/j.lfs.2014.12.012

Statins are competitive inhibitors of HMGCoA reductase and are commonly used as antihypercholesterolemic agents. Experimental studies clearly demonstrate the beneficial effects of statins on bone. Tocotrienols have also been shown to have anti-osteoporotic effects on the skeletal system. This study was conducted to observe the effect of a combination of delta-tocotrienol and lovastatin on structural bone histomorphometry and bone biomechanical strength in a postmenopausal rat model at clinically tolerable doses, and to compare it with the effect of delta-tocotrienol or lovastatin.
Triangulating the pharmacological properties of thymoquinone in regulating reactive oxygen species, inflammation, and cancer: Therapeutic applications and mechanistic pathways

Phua CYH, Teoh ZL, Goh BH, Yap WH, Tang YQ

Life Sci, 2021 Nov 08;287:120120.
PMID: 34762903 DOI: 10.1016/j.lfs.2021.120120

Cancer is a heterogeneous disease with high morbidity and mortality rate involving changes in redox balance and deregulation of redox signalling. For decades, studies have involved developing an effective cancer treatment to combat treatment resistance. As natural products such as thymoquinone have numerous health benefits, studies are also focusing on using them as a viable method for cancer treatment, as they have minimal toxic effects compared with standard cancer treatments. Thymoquinone studies have shown numerous mechanisms of action, such as regulation of reactive species interfering with DNA structure, modulating various potential targets and their signalling pathways as well as immunomodulatory effects in vitro and in vivo. Thymoquinone's anti-cancer effect is mainly due to the induction of apoptotic mechanisms, such as activation of caspases, downregulation of precancerous genes, inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), anti-tumour cell proliferation, ROS regulation, hypoxia and anti-metastasis. Insight into thymoquinone's potential as an alternative treatment for chemoprevention and inflammation can be accomplished via compiling these studies, to provide a better understanding on how and why it works, as well as its interactions with common chemotherapeutic treatments.
Tβ4 ameliorates oxidative damage and apoptosis through ERK/MAPK and 5-HT1A signaling pathway in Aβ insulted SH-SY5Y cells

Zhang GH, Pare RB, Chin KL, Qian YH

Life Sci, 2021 Nov 25.
PMID: 34838849 DOI: 10.1016/j.lfs.2021.120178

AIMS: Alzheimer's disease (AD) is the most common progressive neurodegenerative disorder seriously endangering the physical and mental health of the elderly, while no effective treatments and drugs in clinical practice are available. Thymosin β4 (Tβ4) is a multifunctional polypeptide involved in many physiological and pathological processes including AD. This study aims to understand the function and molecular mechanism of Tβ4 in the development of AD.
MAIN METHODS: Neuroblastoma cell line SH-SY5Y was treated with β-amyloid (Aβ) to induce AD-like pathological changes, which serves as Alzheimer's disease model. Tβ4 was overexpressed in SH-SY5Y cells by lentivirus infection, and downregulated by siRNA transfection. Apoptosis of transfected SH-SY5Y cells after Aβ-treatment was examined by western blot and flow cytometry. Apoptotic proteins and Tβ4-related signaling pathways were also investigated by western blot.
KEY FINDINGS: We found that Tβ4 overexpression increased viability and suppressed apoptosis of Aβ-treated SH-SY5Y cells. Tβ4 ameliorated oxidative damage and suppressed reactive oxygen species production in Aβ-treated SH-SY5Y cells. Consistently, Tβ4 overexpression down-regulated the expression levels of pro-apoptotic markers such as Caspase-3, Caspase-8, and Bax, while up-regulated the expression level of anti-apoptotic gene Bcl-2 in Aβ-stimulated SH-SY5Y cells. Mechanistically, we demonstrated that Tβ4 dampened ERK/p38 MAPK signaling and enhanced 5-HTR1A expression in Aβ-treated SH-SY5Y cells. Moreover, we revealed that Tβ4 inhibited the activation of ERK pathway through up-regulating 5-HTR1A in Aβ-treated SH-SY5Y cells.
SIGNIFICANCE: Taken together, our findings provide evidences to support the neuroprotective role of Tβ4 and might open up new therapeutic applications of Tβ4 in AD treatment.