In this study, the effect of boric acid (BA) on blood sugar levels, vitamins and minerals in Streptozotocin (STZ)-induced diabetes in rats was investigated. In the study, 48 male Wistar albino rats (200-220 g) were divided into 6 groups, no special treatment was administered to Group1, experimental diabetes was induced by administering STZ (45 mg/kg) through intraperitoneal (IP) injection to other groups. Group 2 diabetes; Group 3 (6 U/kg insulin) insulin; Group 4; 250 ppm, group 5; 500 ppm and group 6 1000 ppm BA mixed with their feed. Blood glucose levels of all groups were quantified from blood taken from the tail vein every week. At the end of study, the rats were sacrificed and their blood was taken. The serum levels of vitamins A, E, and minerals were studied. When compared with other groups, blood glucose levels of groups 4, 5 and 6 were found to be increased (p

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent systemic inflammation, which contributes to progressive multi-organ dysfunction, particularly in metabolically active tissues such as the liver and kidneys. Bee bread (Perga), a fermented bee pollen product rich in bioactive compounds, has been reported to exert anti-inflammatory and organ-protective effects; however, its tissue-specific influence on inflammatory responses under diabetic conditions remains incompletely defined. Thirty-two male Wistar Albino rats were randomly assigned to four groups: Control, DM, DM + Perga, and Perga. Diabetes was induced by streptozotocin (STZ; 55 mg/kg, i.p.). Perga was administered orally at a dose of 0.5 g/kg/day for 28 days. Pro-inflammatory cytokine levels (CRP, TNF-α, IL-1β, and IL-6) were quantified in liver and kidney tissues using ELISA. Histopathological alterations were evaluated by hematoxylin and eosin staining. DM significantly increased the IL-1β, IL-6, and CRP levels in hepatic tissue and elevated TNF-α, IL-1β, IL-6, and CRP levels in renal tissue. Perga administration attenuated these inflammatory responses, particularly reducing IL-1β and IL-6 levels in the liver and all measured cytokines in the kidney. Histopathological analyses revealed hepatocyte degeneration and necrosis, sinusoidal dilatation, tubular epithelial degeneration, and glomerular damage in diabetic rats, whereas Perga treatment partially improved hepatic alterations and improved renal structural integrity. These findings indicate that Perga exerts tissue-specific anti-inflammatory and protective effects in experimental diabetes, with a more pronounced impact on renal inflammation than on hepatic responses. Although its effects on hepatic TNF-α and CRP levels were limited, Perga may act as a natural modulator of cytokine-mediated inflammatory processes. Further studies are warranted to elucidate the underlying molecular mechanisms.

Background/Objectives: Autism spectrum disorder (ASD) is a neurodevelopmental condition increasingly associated with dysregulated neuroimmune signaling and altered neurotrophic homeostasis. Tumor necrosis factor-alpha (TNF-α) has been implicated in ASD pathophysiology; however, the downstream effects of TNF-α blockade on cytokine–neurotrophin interactions during neurodevelopment remain insufficiently characterized. In this study, we evaluated the effects of infliximab (IFX), a monoclonal anti-TNF-α antibody, on behavioral performance, neuroinflammatory cytokine profiles, glial activation, and brain-derived neurotrophic factor (BDNF) signaling in a propionic acid (PPA)-induced experimental ASD rat model. Methods: Experimental ASD was induced by propionic acid administration in rats. Animals were divided into control and treatment groups. Behavioral performance was assessed using the Morris Water Maze, direct social interaction, and three-chamber sociability tests. Levels of TNF-α, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and BDNF were measured in serum, hippocampal, and cerebellar tissues. Microglial and astrocytic activation were evaluated using CD11 and GFAP immunohistochemistry. Results: PPA administration resulted in pronounced impairments in learning, memory, and social behaviors, accompanied by elevated proinflammatory cytokine levels, increased BDNF expression, and marked glial activation in the hippocampus and cerebellum. Although IFX treatment significantly reduced TNF-α levels in central tissues, it did not improve behavioral deficits and was associated with persistently elevated IL-1β and IL-6 levels, sustained glial reactivity, and further alterations in BDNF levels. Conclusions: These findings suggest that TNF-α suppression alone does not normalize the disrupted cytokine–neurotrophin axis and may differentially modulate BDNF-related neuroplastic signaling during development. In conclusion, this study indicates that non-selective TNF-α blockade during neurodevelopment fails to confer behavioral benefit in experimental ASD and highlights the importance of considering cytokine–BDNF pathway interactions when designing immunomodulatory strategies for neurodevelopmental disorders.

Ciprofloxacin (CPX) has been associated with neuropsychiatric adverse effects; however, its contribution to depression-like behaviors and the underlying neurobiological mechanisms remain insufficiently characterized. Previous studies have indicated that cinnamic acid (CA) may exert protective actions in the nervous system by modulating oxidative and inflammatory pathways. Nevertheless, its effectiveness in preventing CPX-induced neurobehavioral impairments remains largely unknown. The present study aimed to investigate whether CA attenuates CPX-induced depression-like behaviors through modulation of neuroinflammation and oxidative stress. This study included 60 male Swiss albino mice distributed among six experimental groups (n = 10). Animals were assigned to receive a vehicle, CPX administered at 80 mg/kg, CPX combined with CA at doses of 50, 100, or 200 mg/kg, or CPX together with FLX (20 mg/kg) throughout the 14-day treatment period. Behavioral alterations were assessed using social interaction, forced swimming, tail suspension, and sucrose preference paradigms. In addition, hippocampal and prefrontal cortex tissues were examined for oxidative stress markers (MDA, GSH, and CAT), pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), and neurotransmitters (serotonin, dopamine, and GABA) using ELISA-based assays. CPX administration induced significant depression-like behaviors, evidenced by reduced social interaction, increased immobility, and anhedonia (p < 0.05). These behavioral alterations were associated with increased lipid peroxidation, impaired antioxidant defense, elevated pro-inflammatory cytokine levels, and decreased monoaminergic and GABAergic neurotransmission in both HIP and PFC regions. CA treatment significantly improved CPX-induced behavioral and neurochemical alterations. Among the tested doses, the 100 mg/kg regimen produced the most consistent response, accompanied by reduced neuroinflammatory activity and restoration of neurotransmitter levels, particularly in the hippocampus. In conclusion, CA mitigated CPX-induced behavioral deficits and neurochemical alterations, an effect that may be attributed to its regulatory influence on oxidative stress, neuroinflammatory processes, and neurotransmitter balance within the HIP–PFC pathway. Collectively, the findings indicate that CA may have therapeutic relevance in reducing the neuropsychiatric consequences associated with CPX exposure.

Aim: This study aimed to comparatively evaluate the neuroprotective effects of Borago officinalis (BO) extract and 3,4-dimethoxycinnamic acid (3,4-DMCA) on BDNF/CREB signaling pathways and neurotransmitter systems in a scopolamine (SCP)-induced in vitro Alzheimer’s disease model. Methods: HT22 hippocampal and SH-SY5Y prefrontal neuronal cell lines were used. Cells were divided into control, sham, SCP (2 mM), SCP+BO (15 μg/mL), SCP+3,4- DMCA (25 μM), and SCP+galantamine (1 μM) groups. Following treatment, BDNF, CREB, glutamate, acetylcholinesterase (AChE), acetylcholine (ACh), and norepinephrine (NE) levels were measured using ELISA. Results: SCP exposure significantly decreased BDNF, CREB, ACh, and NE levels and increased glutamate and AChE levels in both cell lines (p0.05). Notably, 3,4-DMCA demonstrated more pronounced effects than BO on selected parameters, with significantly lower AChE levels and higher ACh levels in both cell lines (p