Amygdalin, an Apricot Kernel Extract, Protects Against Keratoconjunctivitis Sicca

by | Jul 8, 2019 | 2019, Eye Health

Written by Angeline A. De Leon, Staff Writer. Apricot kernel extract improved urban particulate matter-induced keratoconjunctivitis sicca in rats by significantly increasing tear volume, inhibiting damage to the corneal epithelium, decreasing corneal surface irregularity, and attenuating disruption of the mucin-4 layer by inhibiting MMP-9, IL-6, and TNF- α.

eye healthKeratoconjunctivitis sicca (KCS), dry eye, is a chronic condition resulting from inadequate production of tears, often leading to discomfort, sensitivity to light, and impaired vision 1,2. Globally, over 30% of individuals experience symptoms of KCS 1 and, subsequently, poorer quality of life 3. Urban particulate matter (UPM), a mixture of solid and liquid particles and a major component of air pollution 4, is thought to contribute to certain respiratory diseases 5 as well as corneal cell inflammation 6. UPM may promote general inflammation and other oxidative processes at the cellular level 5, but its potential role in KCS is not well understood. In the search for herbal treatments for UPM-induced KCS, the apricot kernel (seed of Prunus armeniaca L.) appears to be promising, due to its anti-oxidant and anti-microbial properties 7.  In skin diseases like acne and dandruff, apricot kernel demonstrates the ability to moisturize and lubricate skin 8, and in a previous study has been shown to improve dry eye symptoms in a mouse model 9. Apricot kernel also contains amygdalin, a component known to induce mucin secretion and help maintain mucosal integrity 10. In a 2019 study 11 published in Molecules, researchers in Korea conducted a follow-up study investigating the protective effects of apricot kernel extract (AKE) on UPM-induced KCS in rats.

A group of 6-week-old female Sprague Dawley rats were assigned to one of four groups: a control group; a vehicle group; an AKE-treated group receiving 0.5 mg/mL AKE; an AKE-treated group receiving 1 mg/mL AKE. KCS was induced by topically administering 20 µL UPM onto the eyes of rats (with exception of control group) three times daily for 5 days. Following UPM treatment for 5 days, rats in each group were topically exposed to 20 µL of saline or AKE (0.5 or 1 mg/mL) once daily for 5 days and then tear volume (measure of tear secretion) of the lower eyelid and corneal epithelial damage (based on calculated fluorescein staining score), and corneal irregularity (break in the stability of tear film, based corneal irregularity score) were measured. An in vitro study was also carried out using conjunctival epithelial cells from fetal bovine. Cells were treated with AKE (1, 10, or 100 µg/mL) and amygdalin (0.1, 1, or 10 µg/mL) 1 hour before 100 µg/mL UPM exposure treatment. 24 hours following UPM exposure, activity of matrix metalloproteinases (MMP, group of enzymes involved in protein breakdown) in cell culture media was measured and inflammatory factors (Interleukin-1β, IL-1β; IL-1, tumor necrosis factor-α, TNF-α) were quantified.

Results showed that the decrease in tear volume induced by UPM exposure was significantly attenuated by topical administration of 1 mg/mL AKE (5.0 +/- 0.31 mm, p < 0.01). 1 mg/mL AKE also inhibited corneal epithelial damage (corneal fluorescein staining score: 1.8 +/- 0.25, p < 0.05), and corneal irregularity (corneal irregularity score: 1.5 +/- 0.25, p < 0.05). In vitro results revealed that 10 and 100 µg/mL AKE (p < 0.01 for both) and 1 and 10 µg/mL amygdalin (p < 0.05, p < 0.01, respectively) significantly reduced UPM-induced elevation of MMP activity. Regarding inflammation levels, 10 and 100 µg/mL AKE (p < 0.05, p < 0.01, respectively) and 1 and 10 µg/mL amygdalin (p < 0.01 for both) were seen to significantly decrease UPM-induced increase in TNF- α release. At 100 µg/mL of AKE (p < 0.01) and 10 µg/mL of amygdalin (p < 0.05), UPM-induced increase in IL-6 release was also significantly inhibited.

The present study provides evidence supporting the utility of AKE, as well as its bioactive compound amygdalin, in protecting against symptoms of UPM-induced KCS. By inhibiting damage to the cornea and helping to maintain ocular surface stability, AKE appears to fortify the eye’s natural defense mechanism against environmental insult. The in vitro portion of the present study also indicates that at higher doses, AKE and amygdalin can protect against KCS by attenuating MMP activity and reducing inflammation levels. Overall, AKE and amygdalin, as topical treatments, appear to effectively protect against symptoms of KCS induced by particulate matter. Follow-up studies are needed to confirm the safety and efficacy of AKE in human subjects.

Source: Hyun S, Kim J, Park B., et al. Apricot kernel extract and amygdalin inhibit urban particulate matter-induced keratoconjunctivitis sicca. Molecules. 2019; 24: 650. DOI: 10.3390/molecules 24030650.

© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/

Click here to read the full text study.

Posted July 8, 2019.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

References:

  1. Lemp M, Baudouin C, Baum J, et al. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop (2007). The ocular surface. 2007;5(2):75-92.
  2. Yu G-Y, Zhu Z-H, Mao C, et al. Microvascular autologous submandibular gland transfer in severe cases of keratoconjunctivitis sicca. International journal of oral and maxillofacial surgery. 2004;33(3):235-239.
  3. Janine A. The epidemiology of dry eye disease: report of the epidemiological subcommittee of the international dry eye workshop. The ocular surface. 2007;5(2):93-107.
  4. Schwartz J. Air pollution and daily mortality: a review and meta analysis. Environmental research. 1994;64(1):36-52.
  5. Huang Y-CT, Li Z, Harder SD, Soukup JM. Apoptotic and inflammatory effects induced by different particles in human alveolar macrophages. Inhalation toxicology. 2004;16(14):863-878.
  6. Li J, Tan G, Ding X, et al. A mouse dry eye model induced by topical administration of the air pollutant particulate matter 10. Biomedicine & Pharmacotherapy. 2017;96:524-534.
  7. Yiğit D, Yiğit N, Mavi A. Antioxidant and antimicrobial activities of bitter and sweet apricot (Prunus armeniaca L.) kernels. Brazilian Journal of Medical and Biological Research. 2009;42(4):346-352.
  8. Lee Hh, Ahn JH, Kwon AR, Lee ES, Kwak JH, Min YH. Chemical composition and antimicrobial activity of the essential oil of apricot seed. Phytotherapy research. 2014;28(12):1867-1872.
  9. Kim C-S, Jo K, Lee I-S, Kim J. Topical application of apricot kernel extract improves dry eye symptoms in a unilateral exorbital lacrimal gland excision mouse. Nutrients. 2016;8(11):750.
  10. Nabavizadeh F, Alizadeh AM, Sadroleslami Z, Adeli S. Gastroprotective effects of amygdalin on experimental gastric ulcer: Role of NO and TNF. Journal of Medicinal Plants Research. 2011;5(14):3122-3127.
  11. Hyun S-W, Kim J, Park B, et al. Apricot Kernel Extract and Amygdalin Inhibit Urban Particulate Matter-Induced Keratoconjunctivitis Sicca. Molecules. 2019;24(3):650.