**1. Introduction**

Although medical knowledge and technology have advanced considerably, cerebral ischemic stroke patients experience pain with severe disabilities and high mortality due to brain damage resulting from middle cerebral artery occlusion (MCAo) [1,2]. The progression of pathological changes in acute ischemic stroke includes oxidative stress, free radical production, brain edema, neuronal apoptosis, and finally death [3,4]. Intravenous recombinant tissue plasminogen activator (rtPA) or other agents such as anti-cytokines, calcium channel blockers, and free radical scavengers for therapeutic thrombolysis are the generally applied treatments in the early stage of the disease [5]. However, there is rarely a complete recovery of ischemia neuronal damage. Therefore, in recent years, researchers have recognized the importance of finding inventive strategies for the restoration of brain injury.

Natural derived products, including molecules from marine organisms, have gained recognition as alternative therapeutic sources. The past decade has seen a rise in the application of various compounds from isolated marine species as a popular and promising therapeutic approach for human diseases [6]. Marine organisms are capable of overcoming some insuperable conditions such as light, temperature, pressure, and oxygen and ion concentration due to their distinct habitat environment [7]. Echinochrome A (Ech A), a dark red pigment, is most commonly extracted from the shells, spines, and eggs of sea urchins [8]. The biologically active compound possesses antiviral, antialgal, and

antioxidant properties [8,9]. Ech A is an active substance in the cardioprotective drug Histochrome, registered in Russia (P N002363/01). It presented a positive outcome in animal disease model with experimental hemorrhagic stroke as previously described [10]. Histochrome accelerates the alleviation of neurological symptoms and edema, which are mainly caused by the release of free iron and oxidative stress. The effects of Ech A on ischemic stroke have not been previously studied. In particular, the high antioxidant efficacy exerts a beneficial advantage in the research of stroke [11]. Oxidative stress contributes to irreversible pathophysiological cellular damages during the initial and later phases of ischemic stroke [11]. Despite the restoration of blood flow to rescue the ischemic brain, reperfusion is known to aggravate oxidative stress damage and generate reactive oxygen species (ROS) [12]. Ech A neutralizes the iron cations that accumulate in the region of ischemic damaged tissue [12]. However, researchers have rarely considered Ech A as a therapeutic candidate to overcome brain ischemic stroke.

Based on the results obtained using an experimental rat MCAo model, we demonstrate the potential of Ech A for treating brain ischemic stroke. In the present study, the therapeutic effects of Ech A were evaluated. The administration of Ech A recovered the brain region and alleviated the repressed behaviors in the rat MCAo model. Our results indicate that the administration of Ech A influences the expression of cell viability related factors, thereby confirming its effect on physiological improvements.

#### **2. Results and Discussion**
