Neuroprotective Effects of Musk of Muskrat on Transient Focal Cerebral Ischemia in Rats

Abstract

Musk of musk deer has been one of the most precious traditional medicinal materials for treatment of stroke, but trading is prohibited. Musk of muskrat, Ondatra zibethicus, is an accessible substitute for musk of musk deer. However, neuroprotective effects of the musk of muskrat on stroke model are so far unclear. Aim of the study is to determine neuroprotective effects of the musk of muskrat on focal cerebral ischemia. The protective effects against focal cerebral ischemia were evaluated using a model of middle cerebral artery occlusion (90-minute occlusion followed by 24-hour reperfusion). Musk of muskrat was collected from scent bag of muskrat and orally administered at doses of 100 and 300 mg/kg twice at times of 0 and 90 min after occlusion. The effects on sensorimotor dysfunction were investigated by using balance beam test and rotarod test after brain ischemia. The expression of cyclooxygenase-2 (COX-2) was investigated by immunohistochemistry. Oral administration of musk at 300 mg/kg significantly reduced (p<0.001) the infarct volume by 32.4% compared with a vehicle-treated group. Oral administration of musk at 300 mg/kg also ameliorated ischemia-induced spontaneous and vestibule sensorimotor dysfunction in balance beam test and rotarod test compared with control group and COX-2 upregulation. Musk of muskrat may have neuroprotective effects against transient focal cerebral ischemia with recovery of sensorimotor dysfunction. Regarding the immunohistochemistry, the effects of muskrat may be due to anti-inflammatory properties through inhibition of COX-2 expressions.

Semiochemical responsive olfactory sensory neurons are sexually dimorphic and plastic

“…Our identification of the macrocyclic musk odorant CPD as an agonist for OSNs expressing the male-enriched ORs Olfr1437 and Olfr235 is both intriguing, and consistent, with the previous findings that showed activation of OSNs expressing these receptors by the macrocyclic musk odorant muscone ( McClintock et al, 2014 ; Sato-Akuhara et al, 2016 ). Given the sex-specificity of macrocyclic musk odorants in nature, including in the Moschus (musk deer) and Ondatra (muskrat) species, it has been theorized that this family of odorants may be involved in chemical communication, potentially encoding information about the sex and maturity of an individual ( Li et al, 2016 ; Lee et al, 2019 ). Although we were unable to find any literature of sex-specific macrocyclic musk volatile secretion by Mus musculus , it is tempting to speculate on the existence of a macrocyclic musk molecule, perhaps generated by female mice, that doubles as a semiochemical.…”

Musk (Moschus moschiferus) Attenuates Changes in Main Olfactory Bulb of Depressed Mice: Behavioral, Biochemical, and Histopathological Evidence

“…Similar results were reported by Abd El and Ayuob et al (2016) in the hippocampus of CUMS mice model, which is an important site for postdevelopmental neurogenesis together with MOB. Wang et al (2015) and Lee et al (2019) said that musk also had neuroprotective effect against focal cerebral ischemia in cases of ischemia/reperfusion injury.…”

“…Musk is a part of traditional Chinese medicine as it possesses many beneficial effects such as immunityenhancing, antibacterial, and anti-inflammatory effects (Li et al, 2018;Jie et al, 2019). Adding to that, musk has significant effects on the central nervous system (CNS) as it has been used in treating stroke, coma, neurasthenia, convulsions, and cerebral ischemia (Ayuob, 2017;Abd El Wahab et al, 2018;Lee et al, 2019;Radnaa et al, 2020). Musky compounds, for example, androstadienone, androstenol, and muscone, were described to modulate psychological state, reducing negative mood and increasing positive mood (Jacob and McClintock, 2000;Jacob et al, 2001Jacob et al, , 2002.…”

A Network Pharmacology Approach to Investigate the Active Compounds and Mechanisms of Musk for Ischemic Stroke

“…It can reduce the volume of transient focal cerebral ischemic infarction and improve spontaneous and vestibular sensorimotor dysfunction caused by ischemia. The mechanism is related to inhibiting the expression of COX-2 and exerting an anti-inflammatory response [ 59 ]. TNF is an inflammatory factor produced by activating monocytes or macrophages.…”