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Bipolar disorder (BD) is a chronic mental illness characterized by mood fluctuations that range from depressive lows to manic highs. Several studies have linked the downregulation of SIRT-1 (silent mating type information regulation-2 homologs) signaling to the onset of BD and other neurological dysfunctions. This research aimed to look into the neuroprotective potential of Solanesol (SNL) in rats given ICV-Ouabain injections, focusing on its effect on SIRT-1 signaling activation in the brain. Ouabain, found in hypothalamic and medullary neurons, is an endogenous inhibitor of brain Na+/K+ ATPase. The inhibition of brain Na+/K+ ATPase by Ouabain may also result in changes in neurotransmission within the central nervous system. SNL is a Solanaceae family active phytoconstituent produced from the plant Nicotiana tabacum. SNL is used as a precursor for the production of CoQ10 (Coenzyme Q10), a powerful antioxidant and neuroprotective compound. In the current study, lithium (Li), an important mood stabilizer drug, was used as a control. This study looked at the neuroprotective potential of SNL at dosages of 40 and 80 mg/kg in ICV-OUA injections that caused BD-like neurobehavioral and neurochemical defects in Wistar rats. Wistar rats were placed into eight groups (n = 6) and administered 1 mM/0.5 µL ICV-OUA injections for three days. Neurochemical assessments were done in rat brain homogenates, CSF, and blood plasma samples at the end of the experiment protocol schedule. Long-term SNL and lithium administration have been shown to decrease the number of rearing and crossings and reduce time spent in the center, locomotor activities, and immobility time. Solansesol treatment gradually raises the amount of Na+/K+ ATPase, limiting the severity of behavioural symptoms. These findings also revealed that SNL increases the levels of SIRT-1 in CSF, blood plasma, and brain homogenate samples. Moreover, in rat brain homogenates and blood plasma samples, SNL modulates apoptotic markers such as Caspase-3, Bax (pro-apoptotic), and Bcl-2 (anti-apoptotic). Mitochondrial-ETC complex enzymes, including complex-I, II, IV, V, and CoQ10, were also restored following long-term SNL treatment. Furthermore, SNL lowered inflammatory cytokines (TNF-α, IL-1β) levels while restoring neurotransmitter levels (serotonin, dopamine, glutamate, and acetylcholine) and decreasing oxidative stress markers. Histological examinations also validated Solanesol’s protective effect. As a result, our findings suggest that SNL, as a SIRT-1 signalling activator, may be a promising therapeutic approach for BD-like neurological dysfunctions.

Background Bipolar disorder (BD) is a chronic mental illness characterized by mood fluctuations that range from depressive lows to manic highs. Several studies have linked the downregulation of SIRT-1 (silent mating type information regulation-2 homologs) signaling to the onset of BD and other neurological dysfunctions. The purpose of this research was to look into the neuroprotective potential of Solanesol (SNL) in rats given ICV-Ouabain injections, with a focus on its effect on SIRT-1 signaling activation in the brain. Ouabain, which is found in hypothalamic and medullary neurons, is an endogenous inhibitor of brain Na+/K+ ATPase. The inhibition of brain Na+/K+ ATPase by Ouabain may also result in changes in neurotransmission within the central nervous system. SNL is a Solanaceae family active phytoconstituent produced from the plant Nicotiana tabacum. SNL is used as a precursor for the production of CoQ10 (Coenzyme Q10), a powerful antioxidant and neuroprotective compound. In the current study, lithium (Li), an important mood stabilizer drug, was used as a control. Methods This study looked at the neuroprotective potential of SNL at dosages of 40 and 80 mg/kg in ICV-OUA injections that caused BD-like neurobehavioral and neurochemical defects in Wistar rats. Wistar rats were placed into eight groups (n=6) and administered 1 mM/0.5µl ICV-OUA injections for three days. Neurochemical assessments were done in rat brain homogenates, CSF, and blood plasma samples at the end of the experiment protocol schedule. Results Long-term SNL and lithium administration have been shown to decrease the number of rearing and crossings, as well as reduce time spent in the center, locomotor activities, and immobility time. Solansesol treatment gradually raises the amount of Na+/K+ ATPase, limiting the severity of behavioural symptoms. These findings also revealed that SNL increases the levels of SIRT-1 in CSF, blood plasma, and brain homogenate samples. Furthermore, in rat brain homogenates and blood plasma samples, SNL modulates apoptotic markers such as Caspase-3, Bax (pro-apoptotic), and Bcl-2 (anti-apoptotic). Mitochondrial-ETC complex enzymes, including complex-I, II, IV, V, and CoQ10, were also restored following long-term SNL treatment. Furthermore, SNL lowered inflammatory cytokines (TNF-α, IL-1β) levels while restoring neurotransmitter levels (serotonin, dopamine, glutamate, and acetylcholine) and decreasing oxidative stress markers. Conclusion As a result, our findings suggest that SNL, as a SIRT-1 signalling activator, may be a promising therapeutic approach for BD-like neurological dysfunctions.

Bipolar disorder (BD) is a serious and widespread chronic mental condition characterized by mood swings ranging from depressive lows to manic highs. Several studies have linked SIRT-1 (silent mating type information regulation-2 homologs) signalling downregulation to the progression of BD and other neurological dysfunctions. The purpose of this study was to investigate the neuroprotective potential of solanesol(SNL) in rats with brain intoxication caused by intracerebroventricular (ICV) injections of ouabain(OUA), with a particular focus on its influence on the SIRT-1 signaling activator in the brain. The goal of this study was to investigate the neuroprotective potential of Solanesol (SNL) in rats treated with ICV-OUA injection, with a special emphasis on its effect on the SIRT-1 signalling activation in the brain. Ouabain (OUA) is a cardiac glycoside that inhibits the Na+/K+-ATPase (sodium-potassium adenosine triphosphatase). SNL is an active phytoconstituent belongs to the Solanaceae family, derived from the plant Nicotiana tabacum. SNL is employed as a precursor for the production of CoQ10 (Coenzyme Q10), which has potent antioxidant and neuroprotective properties. Lithium (Li), an important mood stabiliser drug employed as a control in the present study. This study looked at the neuroprotective potential of SNL at doses of 40 and 80 mg/kg in ICV-OUA injections, which caused BD-like neurobehavioral deficits in Wistar rats. Wistar rats were divided into eight groups (n=8) and given 1 mM/0.5 l OUA injections for three days. Long-term SNL and lithium administration can reduce the number of rearing and crossings and time spent in the centre, locomotive activity, and immobility time. According to the findings of this study, SNL increases the levels of SIRT-1 in CSF, blood plasma, and brain homogenate samples. In addition, SNL modulates the apoptotic markers like Caspase-3, Bax (pro-apoptotic), and Bcl-2 (anti-apoptotic) in rat brain homogenates and blood plasma samples. Mitochondrial-ETC complexes enzymes including complex-I, II, IV, V, and CoQ10 were also resorted after the long term administration of SNL. Furthermore, SNL reduced inflammatory cytokines (TNF-α, IL-1β) while restoring neurotransmitter (serotonin, dopamine, glutamate, and acetylcholine) levels and level of oxidative stress markers. Our neurochemical observations could be validated as diagnostic biomarkers in BD-like conditions. As a result, SNL as SIRT-1 signaling activator could be a promising therapeutic target for the treatment of BD.