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Carotenoids are hydrophobic pigments produced exclusively by plants, fungi, and specific microbes. Microalgae are well suited for the production of valuable carotenoids due to their rapid growth, efficient isoprenoid production pathway, and ability to store these compounds within their cells. The possible markets for bio-products range from feed additives in aquaculture and agriculture to pharmaceutical uses. The production of carotenoids in microalgae is affected by several environmental conditions, which can be utilized to enhance productivity. The current study focused on optimizing the extraction parameters (time, temperature, and extraction number) to maximize the yield of carotenoids. Additionally, the impact of various nitrogen sources (ammonia, nitrate, nitrite, and urea) on the production of lutein and loroxanthin in Scenedesmus obliquus was examined. To isolate the carotenoids, 0.20 g of biomass was added to 0.20 g of CaCO3 and 10.0 mL of ethanol solution containing 0.01% (w/v) pyrogallol. Subsequently, the extraction was performed using an ultrasonic bath for a duration of 10 min at a temperature of 30 °C. This was followed by a four-hour saponification process using a 10% methanolic KOH solution. The concentration of lutein and loroxanthin was measured using HPLC–DAD at 446 nm, with a flow rate of 1.0 mL/min using a Waters YMC C30 Carotenoid column (4.6 × 250 mm, 5 μm). The confirmation of carotenoids after their isolation using preparative chromatography was achieved using liquid chromatography–tandem mass spectrometry (LC–MS/MS) with an atmospheric pressure chemical ionization (APCI) probe and UV–vis spectroscopy. In summary, S. obliquus shows significant promise for the large-scale extraction of lutein and loroxanthin. The findings of this study provide strong support for the application of this technology to other species. [ABSTRACT FROM AUTHOR]

Apigenin is a plant flavone proven with biological properties such as anti-inflammatory, antioxidant, and antimicrobial effects. This study, it was aimed to examine the possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of the mild traumatic brain injury (TBI) model. Wistar albino male rats were randomly assigned to groups: control (n = 9), TBI (n = 9), TBI + vehicle (n = 8), and TBI + apigenin (20 and 40 mg/kg, immediately after trauma; n = 6 and n = 7). TBI was performed by dropping a 300 g weight from a height of 1 m onto the skull under anesthesia. Neurological examination and tail suspension tests were applied before and 24 h after trauma, as well as Y-maze and object recognition tests, after that rats were decapitated. In brain tissue, luminol- and lucigenin-enhanced chemiluminescence levels and cytokine ELISA levels were measured. Histological damage was scored. Data were analyzed with one-way ANOVA. After TBI, luminol (p <.001) and lucigenin (p <.001) levels increased, and luminol and lucigenin levels decreased with apigenin treatments (p <.01–.001). The tail suspension test score increased with trauma (p <.01). According to the pre-traumatic values, the number of entrances to the arms (p <.01) in the Y-maze decreased after trauma (p <.01). In the object recognition test, discrimination (p <.05) and recognition indexes (p <.05) decreased with trauma. There was no significant difference among trauma apigenin groups in behavioral tests. Interleukin (IL)-10 levels, one of the anti-inflammatory cytokines, decreased with trauma (p <.05), and increased with 20 and 40 mg apigenin treatment (p <.001 and p <.01, respectively). The histological damage score in the cortex was decreased in the apigenin 20 mg treatment group significantly (p <.05), but the decrease observed in the apigenin 40 mg group was not significant. The results of this study revealed that apigenin 20 and 40 mg treatment may have neuroprotective effects in mild TBI via decreasing the level of luminol and lucigenin and increasing the IL-10 levels. Additionally, apigenin 20 mg treatment ameliorated the trauma-induced cortical tissue damage. [ABSTRACT FROM AUTHOR]

Objective: Traumatic brain injury (TBI) is associated with high mortality and morbidity. Trauma-induced primary damage is followed by apoptosis, lipid peroxidation and oxidative stress that lead to secondary damage, causing exacerbation of TBI. In various inflammation models, dexpanthenol was shown to protect tissues against oxidative damage. It was aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI model. Methods: Wistar albino male rats were randomly assigned to control (n = 8), TBI+dexpanthenol (500 mg/kg; n = 10) and TBI+vehicle (n = 10) groups. TBI was performed under anesthesia (ketamine+xylazine) by dropping a 300 g weight from 70- cm height on the skull of rats, which were injected intraperitoneally with vehicle or dexpanthenol immediately after trauma. At 24th h of trauma, rats were decapitated. Malondialdehyde (MDA) -indicative of lipid peroxidation-, myeloperoxidase (MPO) -marker of neutrophil infiltration-, apoptosis-marker caspase-3, antioxidant superoxide dismutase (SOD) levels and catalase (CAT) activities and levels of luminol- and lucigenimmediated chemiluminescence (CL), -indicating presence of reactive oxygen species- were measured in brain tissues. Following transcardiac parafolmadehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. The data was evaluated by one-way ANOVA. Results: In the vehicle-treated TBI group, MPO level, caspase- 3 activity and luminol-lucigenin CL levels were elevated (p<0.05-0.001), while in the dexpanthenol-treated TBI group these increases were suppressed (p<0.05-0,001) and MDA levels were decreased (p<0.05). Decreased SOD and CAT activities (p<0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol-treated TBI group (p<0.05- 0.001). Neuronal damage observed microscopically in the cortices of TBI was relatively less in the dexpanthenol-treated group. Conclusion: Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and thereby alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI. [ABSTRACT FROM AUTHOR]

Objective: Oxidative stress following traumatic brain injury (TBI) leads to further deterioration of brain damage. Mildronate, known for its vasodilator and anticonvulsant effects, has been shown to be useful in a variety of experimental models and ischemic diseases. In this study, it was aimed to investigate possible antioxidant and neuroprotective effects of mildronate in a rat TBI model. Methods: Under ketamine anesthesia, TBI (n=20) was induced by dropping a metal weight (300 g) from a height of 70 cm on the skull of male Wistar albino rats. Half of the rats was treated intraperitoneally with vehicle, while the other half was treated with mildronate (100 mg/kg) immediately after TBI. Control group (n=8) was not exposed to any trauma. Twenty-four hours after TBI, transcardial paraformaldehyde perfusion was performed and brain injury was graded histopathologically following hematoxylin-eosin staining. Activities of myeloperoxidase (MPO) -marker of neutrophil infiltration-, apoptosis-marker caspase-3, antioxidant superoxide dismutase (SOD) and catalase (CAT), and levels of luminol- and lucigenin-enhanced chemiluminescence (CL) were measured in brain tissues. The data were evaluated by one-way ANOVA. Results: In the mildronate-treated group, the damage in the cerebral cortex that has occurred due to TBI was lighter compared to that of the vehicle-treated TBI group. Antioxidant SOD activity, which was found to be decreased in the brain tissues of the vehicle-treated TBI group (p<0.01), was increased in the group that has received mildronate treatment (p<0.05). Higher levels of CL, increased MPO and caspase-3 activities (p<0.01- 0.001) in the vehicle-treated TBI group were found to be suppressed in the mildronate-treated group (p<0.05-0.001). Conclusion: Suppression of oxidative damage and apoptosis in brain tissues of rats in mildronate-treated TBI group, and alleviation of brain damage by stimulating antioxidant systems suggest that mildronate should be further evaluated for its possible therapeutic effect in traumatic brain injury. [ABSTRACT FROM AUTHOR]