- [Antioxidant] Naringin exhibits strong antioxidant potential.
- [Heart Health]
- Promotes optimal mitochondrial function in the heart muscle.
- Counteracts fructose-induced cardiomyocyte (heart muscle) apoptosis (cell death).
- Prevents Fructose-Induced Cardiac hypertrophy (a thickening of the walls of the heart due to high sugar diet, caused by mitochondrial dysfunction).
- Naringin is able to suppress mitochondrial reactive oxygen species (ROS) production and mitochondrial dysfunction in cardiomyocytes (cardiac muscle cells) exposed to fructose.
- [Lung Health]
- Naringin protects against acrolein-induced pulmonary injuries.
Disease / Symptom Treatment
- Scar Formation (scar tissue)
- Naringin inhibits the development of hypertrophic scars (A hypertrophic scar is a cutaneous condition characterized by deposits of excessive amounts of collagen which gives rise to a raised scar).
- Naringin inhibits the growth and motility of fibroblasts.
- Naringin may be a new drug for the treatment of hypertrophic scars.
- [Lung Cancer]
- [Heart Disease] (Cardiovascular Disease)
Title: Amelioration of High Fructose-Induced Cardiac Hypertrophy by Naringin
Author(s): Jung Hyun Park, Hyeong Jun Ku, Jae Kyeom Kim, Jeen-Woo Park, & Jin Hyup Lee
Institution(s): Department of Food and Biotechnology, Korea University, Sejong, Korea; School of Life Sciences and Biotechnology, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Taegu, Korea; School of Human Environmental Sciences, University of Arkansas, Fayetteville, Arkansas, USA;
Publication: Scientific Reports
Date: June 21, 2018
Abstract: Heart failure is a frequent unfavorable outcome of pathological cardiac hypertrophy. Recent increase in dietary fructose consumption mirrors the rise in prevalence of cardiovascular diseases such as cardiac hypertrophy leading to concerns raised by public health experts. Mitochondria, comprising 30% of cardiomyocyte volume, play a central role in modulating redox-dependent cellular processes such as metabolism and apoptosis. Furthermore, mitochondrial dysfunction is a key cause of pathogenesis of fructose-induced cardiac hypertrophy. Naringin, a major flavanone glycoside in citrus species, has displayed strong antioxidant potential in models of oxidative stress. In this study, we evaluated protective effects of naringin against fructose-induced cardiac hypertrophy and associated mechanisms of action, using in vitro and in vivo models. We found that naringin suppressed mitochondrial ROS production and mitochondrial dysfunction in cardiomyocytes exposed to fructose and consequently reduced cardiomyocyte hypertrophy by regulating AMPK-mTOR signaling axis. Furthermore, naringin counteracted fructose-induced cardiomyocyte apoptosis, and this function of naringin was linked to its ability to inhibit ROS-dependent ATM-mediated p53 signaling. This result was supported by observations in in vivo mouse model of cardiac hypertrophy. These findings indicate a novel role for naringin in protecting against fructose-induced cardiac hypertrophy and suggest unique therapeutic strategies for prevention of cardiovascular diseases.
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Title: Naringin protects acrolein-induced pulmonary injuries through modulating apoptotic signaling and inflammation signaling pathways in mice
Author(s): Jae Kyeom Kim, Jung Hyun Park, Hyeong Jun Ku, Sung Hwan Kim, Ye Jin Lim, Jeen Woo Park, Jin Hyup Lee
Institution(s): School of Human Environmental Sciences, University of Arkansas, Fayetteville, AR 72703, USA b Department of Food and Biotechnology, Korea University, Sejong 30019, South Korea, School of Life Sciences, Kyungpook National University, Taegu, 37224, South Korea
Publication: The Journal of Nutritional Biochemistry
Date: 6 June 2018
Abstract: Acrolein (2-propenal) is ubiquitous in the environment and connections exist between acrolein exposure and lung cancer risk. Here we investigated the effects of naringin on acrolein induced-lung injuries in mice. Male C57BL/6 mice were allocated into four groups: Vehicle group (no acrolein), Naringin only group (80 mg of naringin/kg bw + no acrolein), Acrolein group (ACR group; acrolein), and Naringin + Acrolein group (NAG+ACR group; 80 mg of naringin/kg bw and acrolein). The mice were subjected acute acrolein inhalation (10 ppm for 12 h) in an inhalation chamber and naringin was intraperitoneally administered to the mice one hour before acrolein exposure. The results demonstrated that, in the NAG+ACR group, pulmonary injuries (e.g., airspace enlargement, lung inflammation) were all significantly improved compared to the ACR group. Further, key markers of MAPK signaling (e.g., p-p38, p-JNK), p53 signaling markers (e.g., p-Chk2, p53), NF-κB signaling axis (e.g., IL-1 β, TNF-α), and oxidative damage markers (e.g., GSSG:GSH ratio, oxidative DNA damage) were all effectively mitigated by the naringin treatment. Naringin provided protection against the environmental toxicant, acrolein, in mice lung via modulating MAPK, p53, and NF-κB signaling pathways and our data may provide significant implications considering the prevalence of acrolein.
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Title: Naringin suppresses the growth and motility of hypertrophic scar fibroblasts by inhibiting the kinase activity of Akt
Author(s): Yingli Song, Bingyu Guo, Shudan Ma, Peng Chang, Kai Tao
Institution(s): Reconstructive and Plastic Surgery, The General Hospital of Shenyang Military Region, Shenyang, PR China
Publication: Biomedicine & Pharmacotherapy
Date: September 2018
Abstract: Hypertrophy is a very common pathologic phenomenon of scar hyperplasia after human skin injury and wound healing. In this article, we first proved that naringin could inhibit the proliferation of fibroblasts by MTT experiments. Flow cytometry indicated that naringin could block the cell cycle and promote apoptosis. Transwell experiments showed that naringin could inhibit the motility activity of fibroblasts. We also found that naringin specifically inhibits the kinase activity of Akt and the phosphorylation of Akt in hypertrophic scar fibroblasts by Kinase-Glo, western blot and real-time PCR assays. Subsequently, western blots and real-time PCR indicated that naringin can inhibit phosphorylation of Akt and downstream proteins of Akt. Our data demonstrated that naringin inhibits the development of hypertrophic scars, at least to a certain extent, by its inhibition of Aktp.
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