Herbasense Virgin Cold Pressed Himalayan Bitter Apricot Kernel Oil – Premium Grade Edible Oil

In this study, our behavioral experiments showed that apricot kernel oil treatment increases PWT and PWL while decreasing TWF. The results of biochemical tests showed that apricot kernel oil reduces inflammation and oxidative stress.

The apricot kernel has about 50 % oil. Apricot kernel oil is rich in triacylglycerols (98 %), followed by phospholipids (1.1 %) and free fatty acids (0.2 %). Triacylglycerols containing three oleic acids (35–42 %), linoleic acid and two oleic acids (22–28 %), two linoleic acids and an oleic acid (7–16 %), a linoleic acid, an oleic acid and a palmitic acid, two linoleic acids and a stearic acid (6–7%), and two oleic acids and a palmitic acid (6–10.4 %) are the major triglyceride content of apricot kernel oil. Unsaturated fatty acids, such as oleic acid (18:1) and linoleic acid (18:2), constitute the most reported fatty acids in apricot kernel oil [30].

Oleic acid, a mono-unsaturated fatty acid, has anti-inflammatory effects [31]. Linoleic acid, a polyunsaturated fatty acid, has beneficial effects on oxidative stress and inflammatory responses [32]. Palmitic acid is the most abundant saturated fatty acid in apricot kernel oil.

In addition to the above-mentioned components, apricot kernel oil is a good source of phytosterols, tocochromanols, carotenoids, and polyphenols. Δ7-stigmasterol, β-Sitosterol, campesterol, cholesterol, 24-methylene–cycloartanol, gramisterol, Δ5-avenasterol, Δ7-avenasterol, and citrostadienol are the most important phytosterols. δ-tocopherol, α-tocopherol, and γ-Tocopherol are the major tocochromanols. β-cryptoxanthin, zeaxanthin, Lutein, and β-carotene constitute the most reported carotenoids in apricot kernel oil.

Apricot kernel oil, with its polyphenols, leads to the elimination of free radicals in the body and thus protects it against oxidative stress. Moreover, apricot kernel oil also contains volatile compounds such as furfural, benzaldehyde, 2-methyl-propanal, 2,5-dimethyl-pyrazine, methoxy pyrazine, 2-methyl-butyl aldehyde, nonanal, methylpyrazine, and 3-ethyl-2,5-dimethyl-pyrazine. However, the major volatile constituent is benzaldehyde [30]. Phytochemicals such as carotenoids, and polyphenolic compounds showed antinociceptive effects in animal models of neuropathic pain [33,34]. Chronic neuropathic pain, which is characterized by an abnormally increased sensitivity to pain.

(hyperalgesia), the perception of harmless stimuli as painful (allodynia), and spontaneous pain, can be caused by damage to the nervous system. The brain and spinal cord’s processing neurons undergo secondary alterations due to the hyperactivity of nociceptors, which causes mechanoreceptive A-fiber input to be interpreted as pain. Additional hyperexcitability may result from neuroplasticity alterations in the central pain modulatory systems. The sensitization of primary afferent nociceptors is caused by molecular mechanisms that include growth factor release from degenerating nerve fibers, upregulation of voltage-gated sodium channels, and different types of receptor proteins. There is evidence of sensitization of brain neurons as well as significant secondary alterations in the spinal cord dorsal horn due to peripheral nociceptor hyperactivity [35].

We chose the CCI model for the surgery of the sciatic nerve and the establishment of neuropathic pain because it is a commonly accepted model for producing reliable resemblances between clinical manifestations of neuropathic pain [36]. The CCI model in our rats successfully exhibited allodynia and hyperalgesia. Apricot kernel oil and gabapentin reduced the allodynia and hyperalgesia at different times of the experiment.

Gabapentin is an anti-epileptic medication but it is used as a first-line therapy in the treatment of neuropathic pain [37]. In our study gabapentin treatment reduced the pain behavior, oxidative stress, and inflammation in neuropathic rats.

It has been shown that proinflammatory and inflammatory cytokines like IL-1β, interferon-gamma (IFN-y), IL-6, and TNF-α can increase spinal neuroinflammatory and immunological activity. It is these events that greatly contribute to the initiation and development of neuropathic pain after a nerve injury [[38], [39], [40]]. In confirmation, studies have demonstrated that reducing the TNF-α, and IL-1β produces pain-relieving effects [41,42].