Gow-Chin Yen

@nchu.edu.tw

Professor, Department of Food Science and Biotechnology
National Chung Hsing University



        

https://researchid.co/gcyen
325

Scopus Publications

Scopus Publications

  • High glucose reduces Nrf2-dependent cRAGE release and enhances infl ammasomedependent IL-1β production in monocytes: the modulatory effects of EGCG
    Chi-Hao Wu, Yin-Hsuan Chang, Chin-Lin Hsu, Sheng-Yi Chen, and Gow-Chin Yen
    Tsinghua University Press



  • Effect of Indian gooseberry extract on improving methylglyoxal-associated leptin resistance in peripheral tissues of high-fat diet-fed rats
    Sheng-Yi Chen, Yue-Ning Huang, Jer-An Lin, and Gow-Chin Yen
    The Journal of Food and Drug Analysis (JFDA), Food and Drug Administration, Taiwan (TFDA)
    Increased leptin resistance and methylglyoxal (MG) levels are observed in obese patients. However, whether MG deposits contribute to leptin resistance, oxidative stress, and inflammation in peripheral tissues remains unclear. In addition, the edible fruit of Indian gooseberry (Phyllanthus emblica L.) contains abundant bioactive components such as vitamin C, β-glucogallin (β-glu), gallic acid (GA), and ellagic acid (EA). Water extract of Indian gooseberry fruit (WEIG) and GA has been shown to improve cognitive decline by suppressing brain MG-induced insulin resistance in rats administered a high-fat diet (HFD). Accordingly, this study investigated the functions of WEIG and GA in inhibiting MG-induced leptin resistance, oxidative stress, and inflammation in the peripheral tissues of HFD-fed rats. The results showed that MG, advanced glycation end products (AGEs), and leptin resistance accumulation in the liver, kidney, and perinephric fat were effectively restored by elevated glyoxalase-1 (Glo-1) activity after WEIG and GA administration comparable to that of alagebrium chloride (positive control) treatment in HFD-fed rats. Furthermore, WEIG and GA supplementation increased adiponectin and antioxidant enzymes (glutathione peroxidase, superoxide dismutase, catalase) and decreased inflammatory cytokines (IL-6, IL-1β, TNF-α) in the peripheral tissues of HFD-fed rats. In conclusion, these findings demonstrated that MG may trigger leptin resistance, oxidative stress, and inflammation in peripheral tissues, which could be abolished by WEIG and GA treatment. These results show the potential of P. emblica for functional food development and improving obesity-associated metabolic disorders.




  • Phyllanthus emblica L. extract alleviates leptin resistance and lipid accumulation by inhibiting methylglyoxal production
    Yue-Ning Huang, Sheng-Yi Chen, Jer-An Lin, I-Chen Chiang, and Gow-Chin Yen
    Elsevier BV

  • Preventive Effect of Indian Gooseberry (Phyllanthus emblica L.) Fruit Extract on Cognitive Decline in High-Fat Diet (HFD)-Fed Rats
    Ying‐Yin Chen, Sheng‐Yi Chen, Jer‐An Lin, and Gow‐Chin Yen
    Wiley
    SCOPE Methylglyoxal (MG)-derived advanced glycation end products (AGEs) directly bind to the receptor for advanced glycation end products (RAGE), subsequently exacerbating obesity and obesity-induced cognitive decline. Indian gooseberry (Phyllanthus emblica L.) fruit has antiobesity properties. However, the underlying mechanism by which Indian gooseberry fruit prevents obesity-induced cognitive decline remains unclear. METHODS AND RESULTS This study aimed to investigate the preventive effect of a water extract of Indian gooseberry fruit (WEIG) and its bioactive compound gallic acid (GA) on the obesity-induced cognitive decline through MG suppression and gut microbiota modulation in high-fat diet (HFD)-fed rats. Trapping MG, WEIG, and GA significantly ameliorated fat accumulation in adipose tissue and learning and memory deficits. Mechanistically, WEIG and GA administration effectively reduced brain MG and AGE levels and subsequently reduced insulin resistance, inflammatory cytokines, MDA production, and Alzheimer's disease-related proteins, but increased both antioxidant enzyme activities and anti-inflammatory cytokine with inhibiting RAGE, MAPK, and NF-κB levels in HFD-fed rats. Additionally, WEIG and GA supplementation increased the relative abundances of Bacteroidetes, Gammaproteobacteria, and Parasutterella, which negatively correlate with MG, inflammatory cytokine, and Alzheimer's disease-related protein expressions. CONCLUSION This novel finding provides a possible mechanism by which WEIG prevents obesity-induced cognitive decline through the gut-brain axis. This article is protected by copyright. All rights reserved.

  • Ameliorative effect of buckwheat polysaccharides on colitis via regulation of the gut microbiota
    Jhih-Yi Yang, Sheng-Yi Chen, Yen-Hsien Wu, Yi-Lun Liao, and Gow-Chin Yen
    Elsevier BV


  • How to deal with frenemy NRF2: Targeting NRF2 for chemoprevention and cancer therapy
    Ya-Chu Tang, Yung-Jen Chuang, Hsin-Huei Chang, Shin-Hun Juang, Gow-Chin Yen, Jang-Yang Chang, and Ching-Chuan Kuo
    The Journal of Food and Drug Analysis (JFDA), Food and Drug Administration, Taiwan (TFDA)
    Induction of antioxidant proteins and phase 2 detoxifying enzymes that neutralize reactive electrophiles are important mechanisms for protection against carcinogenesis. Normal cells provide multifaceted pathways to tightly control NF-E2-related factor 2 (NRF2)-mediated gene expression in response to an assault by a range of endogenous and exogenous oncogenic molecules. Transient activation of NRF2 by its activators is able to induce ARE-mediated cytoprotective proteins which are essential for protection against various toxic and oxidative damages, and NRF2 activators thereby have ef fi cacy in cancer chemoprevention. Because NRF2 has a cytoprotective function, it can protect normal cells from carcinogens like an angel, but when the protective effect acts on cancer cells, it will give rise to invincible cancer cells and play a devilish role in tumor progression. Indeed, aberrant activation of NRF2 has been found in a variety of cancers that create a favorable environment for the proliferation and survival of cancer cells and leads to drug resistance, ultimately leading to the poor clinical prognosis of patients. Therefore, pharmacological inhibition of NRF2 signaling has emerged as a promising approach for cancer therapy. This review aims to compile the regulatory mechanisms of NRF2 and its double-edged role in cancer. In addition, we also summarize the research progress of NRF2 modulators, especially phytochemicals, in chemoprevention and cancer therapy.


  • Rhinacanthus nasutus and okara polysaccharides attenuate colitis via inhibiting inflammation and modulating the gut microbiota
    Sheng‐Yi Chen, Yu‐Chieh Shen, Jer‐An Lin, and Gow‐Chin Yen
    Wiley
    Plant polysaccharides have prebiotic properties for gut microbiota and immune modulation. This study aimed to investigate the prevention abilities of edible Rhinacanthus nasutus polysaccharide (RNP) and okara polysaccharide (OP) in Sprague-Dawley rats with acetic acid-induced colitis. The characterizations of RNP and OP were analyzed, including Fourier transform infrared, thermogravimetric analysis, differential scanning calorimetry, and monosaccharide composition. The prebiotic properties of RNP and OP were determined in vitro. In addition, the pathological features of colon length and inflammatory cytokine levels in acetic acid-induced colitis were improved by intragastric preadministration of RNP and OP for 3 weeks. There was no nephrotoxicity or hepatotoxicity in rats via histopathological assessment after RNP and OP intake. Moreover, the abundance of short-chain fatty acids-producing bacteria (Lachnospiraceae, Lactobacilli, and Prevotellaceae) were increased after RNP supplementation. In conclusion, intragastric gavage of RNP and OP significantly modulated the gut microbiota and immune response, consequently alleviating the symptoms of colitis. This novel finding provides an alternative strategy and potential application of these two polysaccharides for colitis prevention and treatment.

  • Anti-fatigue effects of enzyme-hydrolyzed okara in C2C12 myotubes and Sprague-Dawley rats
    Yu-Jou Chien, Gow-Chin Yen, Shih-Chien Huang, Shiuan-Chih Chen, and Chin-Lin Hsu
    Royal Society of Chemistry (RSC)
    Okara protein hydrolysate (OPH) could exert anti-fatigue effects both in vivo and in vitro through an improvement in mitochondrial function.


  • Protective effects of camellia and olive oils against cognitive impairment via gut microbiota-brain communication in rats
    Sheng-Yi Chen, Ming-Hung Weng, Zih-Ying Li, Guan-Yu Wang, and Gow-Chin Yen
    Royal Society of Chemistry (RSC)
    The camellia oil (PCO) and olive oil consumption effectively improved mild cognitive impairment (MCI) by altering the relationship between the biochemical parameters and gut microbiota; PCO treatment in particularly.


  • 4-Acetylantroquinonol B enhances cell death and inhibits autophagy by downregulating the PI3K/Akt/MDR1 pathway in gemcitabine-resistant pancreatic cancer cells
    Ying-Yin Chen, Sheng-Yi Chen, Tsung-Ju Li, Ting-Wei Lin, Chin-Chu Chen, and Gow-Chin Yen
    Spandidos Publications
    Gemcitabine (GEM) is a typical chemotherapeutic drug used to treat pancreatic cancer, but GEM resistance develops within weeks after chemotherapy. Hence, the development of a new strategy to overcome drug resistance is urgent. 4-Acetylantroquinonol B (4-AAQB), a ubiquinone derived from Taiwanofungus camphoratus, has hepatoprotective, anti-obesity, and antitumor activities. However, the role of 4-AAQB in enhancing GEM sensitivity is unclear. This study aimed to determine the underlying mechanisms by which 4-AAQB enhances cytotoxicity and GEM sensitivity. Cell viability was dramatically reduced by 4-AAQB (2 and 5 µM) treatment in the MiaPaCa-2 and GEM-resistant MiaPaCa-2 (MiaPaCa-2GEMR) human pancreatic cancer cells. 4-AAQB led to cell cycle arrest, upregulated the levels of reactive oxygen species (ROS), promoted apoptosis, and inhibited autophagy, which subsequently enhanced GEM chemosensitivity by suppressing the receptor for advanced glycation end products (RAGE)/high mobility group box 1 (HMGB1)-initiated PI3K/Akt/multidrug resistance protein 1 (MDR1) signaling pathway in both cell lines. Vascular endothelial growth factor A (VEGFA) expression, cell migration, and invasion were also inhibited by the 4-AAQB incubation. Overall, this combination treatment strategy might represent a novel approach for GEM-resistant pancreatic cancer.

  • Lucidone inhibits autophagy and MDR1 via HMGB1/RAGE/PI3K/Akt signaling pathway in pancreatic cancer cells
    Sheng‐Yi Chen, Yi‐Hao Hsu, Sheng‐Yang Wang, Ying‐Yin Chen, Cheng‐Jie Hong, and Gow‐Chin Yen
    Wiley
    Gemcitabine (GEM) drug resistance remains a difficult challenge in pancreatic ductal adenocarcinoma (PDAC) treatment. Therefore, identifying a safe and effective treatment strategy for PDAC is urgent. Lucidone is a natural compound extracted from the fruits of Lindera erythrocarpa Makino. However, the role of lucidone in PDAC inhibition remains unclear. In addition, high-mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) are involved in multidrug resistance protein 1 (MDR1) regulation and GEM resistance. Thus, this study aimed to explore the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of RAGE-initiated signaling in PDAC cells. The data showed that lucidone significantly promoted apoptotic cell death and inhibited the expression of autophagic proteins (Atg5, Beclin-1, LC3-II, and Vps34) and MDR1 by inhibiting the HMGB1/RAGE/PI3K/Akt axis in both MIA Paca-2 cells and MIA Paca-2GEMR cells (GEM-resistant cells). Notably, convincing data were also obtained in experiments involving RAGE-specific siRNA transfection. In addition, remarkable cell proliferation was observed after treatment with lucidone combined with GEM, particularly in MIA Paca-2GEMR cells, indicating that lucidone treatment enhanced chemosensitivity. Collectively, this study provided the underlying mechanism by which lucidone treatment inhibited HMGB1/RAGE-initiated PI3K/Akt/MDR1 signaling and consequently enhanced chemosensitivity in PDAC.

  • The next generation beneficial actions of novel probiotics as potential therapeutic targets and prediction tool for metabolic diseases
    Hsin-Lin Cheng, Gow-Chin Yen, Shih-Chien Huang, Shiuan-Chih Chen, and Chin-Lin Hsu
    The Journal of Food and Drug Analysis (JFDA), Food and Drug Administration, Taiwan (TFDA)
    The prevalence of metabolic disease has rising and affected over 1,000 million populations globally. Since the metabolic disease and its related complication are board, it has become the major health hazard of modern world. However, Long term medication of metabolic disease may cause serious side effects and risk for adverse health problems. Recently, emerging studies focus on exploring the mechanistic details of metabolic state in disease development and progression. Gut bacteria ecosystem was considered to play a pivotal role in regulating energy homeostasis and great associated with the development of metabolic disease. Accumulated evidences indicated that Akkermansia muciniphila, Faecalibacterium prausnitzii, and Roseburia hominis improve the balance of the microecology in the intestine of the host and have positive effects on enhancing nutrients absorption. Hence, the novel probiotics as therapeutic target to modify gut microbiota generally focus on improving microbiota dysbiosis, and offers new prospects for treating metabolic disease. In the present review, we discuss the significant roles and regulatory properties of specific bacterium in the context of intestinal microbial balance, explores the kinds of harmful/beneficial bacteria that were likely to act as indicator for metabolic disease. Further proposed a stepwise procedure in the basis of sequencing technology with that of innovative option to reestablish the microbial equilibrium and prevent metabolic disease.


  • Authentication of dark brown sugars from different processing using three-dimensional fluorescence spectroscopy
    Jui-Yi Chen, Xin-Wei Chen, Yu-Yu Lin, Gow-Chin Yen, and Jer-An Lin
    Elsevier BV

  • Risk and Benefit of Natural and Commercial Dark Brown Sugars as Evidenced by Phenolic and Maillard Reaction Product Contents
    Jui-Yi Chen, Gow-Chin Yen, Nien-Ting Tsai, and Jer-An Lin
    American Chemical Society (ACS)
    Products of dark brown sugar (DBS) from different production processes and raw materials may bring different risks and benefits to human health. Therefore, this study was aimed to evaluate the quality of natural and commercial DBS products. Results showed that physicochemical properties, including pH value, turbidity, and browning degree have no significant difference between natural and commercial DBS products. Total flavonoid content of natural DBS was found to be significantly higher than that of commercial DBS (p < 0.05). Notably, the levels of harmful Maillard reaction products in natural DBS were significantly lower than that in commercial DBS as evidenced by analyses of methylglyoxal and fluorescent advanced glycation end products (p < 0.05). However, the amount of acrylamide in natural DBS was significantly higher than that in commercial DBS. In conclusion, this study provides useful information for risk-benefit assessment of DBS products, which is helpful for food safety management.

  • Effects of Hsian-tsao (: Mesona procumbens Hemsl.) extracts and its polysaccharides on the promotion of wound healing under diabetes-like conditions
    Siao-Ling Fan, Jer-An Lin, Sheng-Yi Chen, Jia-Hong Lin, Hsin-Tang Lin, Ying-Yin Chen, and Gow-Chin Yen
    Royal Society of Chemistry (RSC)
    Hsian-tsao extracts and its polysaccharides accelerate wound healing in cell models and diabetic mice.