Pear Formula for Respiratory Care

Ping Lin¹, Kai-Wen Kan², Jia-Haur Chen², Yung-Kai Lin³, Yung-Hao Lin⁴, Yung-Hsiang Lin¹ and Chen-Meng Kuan^1,

¹Research & Design Center, TCI CO., Ltd., Taipei, Taiwan

²Research & Design Center, TCI Gene Inc., Taipei, Taiwan

³Department of Animal Science, Chinese Culture University, Taipei, Taiwan

⁴Global Business Center, TCI CO., Ltd., Taipei, Taiwan

Cite this paper:
Ping Lin, Kai-Wen Kan, Jia-Haur Chen, Yung-Kai Lin, Yung-Hao Lin, Yung-Hsiang Lin and Chen-Meng Kuan. Pear Formula for Respiratory Care. Journal of Food and Nutrition Research. 2020; 8(3):155-159. doi: 10.12691/jfnr-8-3-6

Abstract

This study unveils the possibility of a pear-based formula for reparatory care. Pears contain abundant polyphenols and triterpenoids in their fruit and skin, which confer antoxidative and anti-inflammatory effects on the prevention of chronic diseases. Pears have been used in several traditional remedies for reliving respiratory syndromes and constipation for over 2000 years in China. However, the use of pears for daily care is not easily accessible for most people. A pear-based sachet is a convenient approach to the beneficial ingredients of pears. The pear-based formula here enhanced wound healing rate by 27% and significantly improved the expression of allergy-, lung disease-, and DNA repair-related genes in lung cells. Moreover, the formula could increase the phagocytic activity of macrophages by 43%. In short, pear-based formula might provide the comprehensive respiratory care as evidenced by improvement in the wound healing efficiency of lung cells, the phagocytic activity of macrophages, down-regulation of the expression of respiratory disease-associated genes, and up-regulation the expression of DNA mismatch repair genes in cellular models.

Keywords:
pear antioxidation phagocytosis mismatch DNA repair wound healing

This work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Figures

References:

[1]	Reiland, H., & Slavin, J. (2015). Systematic review of pears and health. Nutrition Today, 50, 301-305.
[2]	Li, X., Zhang, J. Y., Gao, W. Y., Wang, Y., Wang, H. Y., Cao, J. G., … Huang, L. Q. (2012). Chemical composition and anti-inflammatory and antioxidant activities of eight pear cultivars. Journal of Agricultural and Food Chemistry, 60, 8738-8744.
[3]	Chen, J., Wang Z., Wu, J., Wang, Q., & Hu, X. (2007). Chemical compositional characterization of eight pear cultivars grown in China. Food Chemistry, 104, 268-275.
[4]	Slavin, J. L., & Lloyd, B. (2012). Health benefits of fruits and vegetables. Advances in Nutrition, 3, 506-516.
[5]	Li, X., Gao, W. Y., Huang, L. J., Zhang, J. Y., & Guo, X. H. (2011). Antioxidant and antiinflammation capacities of some pear cultivars. Journal of Food Science, 76, 985-990.
[6]	Cui, T., Nakamura, K., Ma, L., Li, J. Z., Kayahara, H. (2005), Analyses of arbutin and chlorogenic acid, the major phenolic constituents in Oriental pear. Journal of Agricultural and Food Chemistry, 53, 3882-3887.
[7]	Pandey, K. B., & Rizvi, S. I. (2009). Plant polyphenols as dietary antioxidants in human health and disease. Oxidative Medicine and Cellular Longevity, 2, 270-278.
[8]	Sanchez, A. C. G., Gil-Izquierdo, A., & Gil, M. I. (2003). Comparative study of six pear cultivars in terms of their phenolic and vitamin C contents and antioxidant capacity. Journal of Agricultural and Food Chemistry, 83, 995-1003.
[9]	Hwang, S. J., Kim, Y. W., Park, Y., Lee, H. J., & Kim, K. W. (2014). Anti-inflammatory effects of chlorogenic acid in lipopolysaccharide-stimulated RAW 264.7 cells. Inflammation Research, 63, 81-90.
[10]	Shan, J., Fu, J., Zhao, Z., Kong, X., Huang, H., Luo, L., … Yin, Z. (2009). Chlorogenic acid inhibits lipopolysaccharide-induced cyclooxygenase-2 expression in RAW264.7 cells through suppressing NF-κB and JNK/AP-1 activation. International Immunopharmacology, 9, 1042-1048.
[11]	Xiao, L., Matsubayashi, K., & Miwa, N. (2007). Inhibitory effect of the water-soluble polymer-wrapped derivative of fullerene on UVA-induced melanogenesis via downregulation of tyrosinase expression in human melanocytes and skin tissues. Archives of Dermatological Research, 299, 245-257.
[12]	Lee, H. J., & Kim, K. W. (2012). Anti-inflammatory effects of arbutin in lipopolysaccharide-stimulated BV2 microglial cells. Inflammation Research, 61, 817-825.
[13]	Omori, A., Yoshimura, Y., Deyama, Y., & Suzuki, K. (2015). Rosmarinic acid and arbutin suppress osteoclast differentiation by inhibiting superoxide and NFATc1 downregulation in RAW 264.7 cells. Biomedical Reports, 3, 483-490.
[14]	Yadav, V. R., Prasad, S., Sung, B., Kannappan, R., & Aggarwal, B. B. (2010). Targeting inflammatory pathways by triterpenoids for prevention and treatment of cancer. Toxins (Basel), 2, 2428-2466
[15]	Zhang, F., Daimaru, E., Ohnishi, M., Kinoshita, M., & Tokuji, Y. (2013). Oleanolic acid and ursolic acid in commercial dried fruits. Food Science and Technology Research, 19, 113-116.
[16]	Pathak, A. K., Bhutani, M., Nair, A. S., Ahn, K. S., Chakraborty, A., Kadara, H., …Aggarwal, B .B. (2007). Ursolic acid inhibits STAT3 activation pathway leading to suppression of proliferation and chemosensitization of human multiple myeloma cells. Molecular Cancer Research, 5, 943-955.
[17]	Li, L., Lin, J., Sun, G., Wei, L., Shen, A., Zhang, M., … Peng, J. (2016). Oleanolic acid inhibits colorectal cancer angiogenesis in vivo and in vitro via suppression of STAT3 and Hedgehog pathways. Molecular Medicine Reports, 13, 5276-5282.
[18]	WHO (2018). Ambient (outdoor) air pollution. World Health Organization. Retrieved from https://www.who.int/airpollution/en/.
[19]	Hiraiwa, K., & van Eeden, S. F. (2013). Contribution of lung macrophages to the inflammatory responses induced by exposure to air pollutants. Mediators of Inflammation, 2013, 619523
[20]	Bathmanabhan, S., & Madanayak, S. N. S. (2010). Analysis and interpretation of particulate matter-PM10, PM2.5 and PM1 emissions from the heterogeneous traffic near an urban roadway. Atmospheric Pollution Research, 1, 184-194.
[21]	Huang, Y. C., Li, Z., Harder, S. D., & Soukup, J. M. (2004). Apoptotic and inflammatory effects induced by different particles in human alveolarmacrophages. Inhalation Toxicology, 16, 863-878.
[22]	Hogg, J. C., & van Eeden, S. (2009). Pulmonary and systemic response to atmospheric pollution. Respirology, 14, 336-346.
[23]	van Eeden, S. F., & Hogg, J. C. (2002). Systemic inflammatory response induced by particulate matter air pollution: the importance of bone-marrow stimulation. Journal of Toxicology and Environmental Health, Part A, 65, 1597-1613.
[24]	Crosby, L. M., & Waters, C. M. (2010). Epithelial repair mechanisms in the lung. American Journal of Physiology-Lung Cellular and Molecular Physiology, 298, 715-731.
[25]	Bao, Z. J., Fan, Y . M., Cui, Y. F., Sheng, Y. F., & Zhu, M. (2017). Effect of PM2.5 mediated oxidative stress on the innate immune cellular response of Der p1 treated human bronchial epithelial cells. European Review for Medical and Pharmacological Sciences, 21, 2907-2912.
[26]	Huang, H. C., Lin, F. C., Wu, M. F., Nfor, O. N., Hsu, S. Y., … Liaw, Y. P. (2019). Association between chronic obstructive pulmonary disease and PM2.5 in Taiwanese nonsmokers. International Journal of Hygiene and Environmental Health, 222, 884-888.
[27]	Mehlhop, P. D., van de Rijn, M., Brewer, J. P., Kisselgof, A. B., Geha, R. S., Oettgen, H. C., … Martin, T. R. (2000). CD40L, but Not CD40, is required for allergen-induced bronchial hyperresponsiveness in mice. American Journal of Respiratory Cell and Molecular Biology, 23, 646-651.
[28]	Wu, J., Shi, Y., Asweto, C.O., Feng, L., Yang, X., Zhang, Y., … Sun, Z. (2017). Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells. Environmental Science and Pollution Research, 24, 25071-25081.
[29]	Jones, A. C., Troy, N. M.,White, E., Hollams, E. M., Gout, A. M., Ling, K. M. … Bosco, A. (2018). Persistent activation of interlinked type 2 airway epithelial gene networks in sputum-derived cells from aeroallergen-sensitized symptomatic asthmatics. Scientific Reports, 8, 1511.
[30]	Alfaidi, M., Acosta, C. H., Lindquist, J. M., Cockerham, E. D., & Orr, A.W. (2019). The differential roles of the adaptor proteins Nck1 and Nck2 in shear stress-induced endothelial activation. bioRxiv 668129.
[31]	Jiang, L. P., Fan, S. Q., Xiong, Q. X., Zhou,Y. C., Yang, Z. Z., Li, G. F., … Chen, Y. B. (2018). GRK5 functions as an oncogenic factor in non-small-cell lung cancer. Cell Death & Disease, 9, 295.
[32]	Guan, F., Wang, L., Hao, S., Wu, Z., Bai, J., Kang, Z., …Zhang, J. (2017). Retinol dehydrogenase-10 promotes development and progression of human glioma via the TWEAK-NF-κB axis. Oncotarget, 8, 105262-105275.
[33]	Niu, N., Schaid, D. J., Abo, R. P., Kalari, K., Fridley, B. L., Feng, Q., …Wang L. (2012). Genetic association with overall survival of taxane-treated lung cancer patients—A genome-wide association study in human lymphoblastoid cell lines followed by a clinical association study. BMC Cancer, 12, 422.
[34]	Fuentes-Mattei, E., Rivera, E., Gioda, A., Sanchez-Rivera, D., Roman-Velazquez, F.R., & Jimenez-Velez, B. D. (2010). Use of human bronchial epithelial cells (BEAS-2B) to study immunological markers resulting from exposure to PM 2.5 organic extract from Puerto Rico. Toxicology and Applied Pharmacology, 243, 381-389.
[35]	Weeks, L. D., Zentner, G. E., Scacheri, P. C., & Gerson, S. L. (2014). Uracil DNA glycosylase (UNG) loss enhances DNA double strand break formation in human cancer cells exposed to pemetrexed. Cell Death & Disease, 5, e1045.
[36]	Chevillard, S., Radicella, J., Levalois, C., Lebeau, J., Poupon, M., Oudard, S., …Boiteux, S. (1998). Mutations in OGG1, a gene involved in the repair of oxidative DNA damage, are found in human lung and kidney tumours. Oncogene, 16, 3083-3086.
[37]	Sun, S., Liu, Y., Eisfeld, A. K., Zhen, F., Jin, S. Gao, W., …Chen, W. (2019). Identification of germline mismatch repair gene mutations in lung cancer patients with paired tumor-normal next generation sequencing: a retrospective study. Frontiers in Oncology, 9, 550.