Background: Lead acetate (Pb) exposure during frontal cortex development is associated with developmental
toxicity later in life, causing both morphological and functional alterations. Curcuma longa,
however, has been suggested to possess neuroprotective qualities that could lessen these adverse effects.
Objective: Assessed the frontal cortex following treatment with Curcuma longa. Materials and Methods:
Twenty adult female Wistar rats and ten adult male Wistar rats were matched during the proestrous phase
of the estrous cycle in order to mate and create five groups of six (n=6) in a 4:2 (4 females to 2 males)
ratio. Gestational day 0 was marked as the confirmation of pregnancy based on if sperm is present and a
vaginal plug in the vaginal smear. Four (n=4) pregnant Wistar rats were put together. Group 1 (control) rats
were given 2 milliliters per kilogram of distilled water. Pb was given at a dose of 120 mg/kg to Group 2.
Group 3 rats were given 120 mg/kg of lead and 100 mg/kg of vitamin C. The animals in Group 4 received
750 mg/kg of Curcuma longa and 120 mg/kg of Pb. The animals in Group 5 rats were given 1500 mg/kg
of Curcuma longa and 120 mg/kg of Pb. From gestational day 7 to day 21 (14 days), the medication was
administered orally. The animals were allowed to litter naturally. At postnatal day (PND) 1, some pups
were euthanized using chloroform inhalation and their brains were harvested for Oxidative stress markers,
histology, histochemical assessments. While some pups were kept for Cliff avoidance test at PND 4-7.
Results: The study found that lead acetate (Pb) exposure during gestation significantly decreased the mean
turning latency in the cliff avoidance test and increased lipid peroxidation (MDA) levels, while decreasing
antioxidant enzyme levels (SOD, CAT, GSH) compared to the control group. These neurological and oxidative
changes were mitigated by co-administration of Curcuma longa, with a notable improvement in the
cliff avoidance test performance and restoration of the altered histological and histochemical markers. The
results suggest that Curcuma longa, a natural antioxidant, has neuroprotective properties that can counteract
the adverse effects of lead toxicity during gestational development. Conclusion: N-Butanol Fraction
of Curcuma Longa ameliorated lead-induced neurotoxicity in rat pups.

Background: Heavy metals such as lead are ubiquitous elements at exposure causing deleterious
effects on the brain and leading to neurodegenerative diseases. Aim: In this investigation, the
neurotherapeutic effects of ethanol extract of Curcuma longa (EECl) against lead‑induced hippocampal
neurotoxicity in rats were examined. Biochemical examination for antioxidant enzyme activity and
lipid peroxide level (malondialdehyde [MDA], superoxide dismutase [SOD], and glutathione [GSH])
was evaluated, the Barnes maze for learning and memory, and histological analysis (H and E stain)
for general histoarchitectural features to investigate the neurotherapeutic characteristics of EECl.
Materials and Methods: Six groups totalling 36 rats were created (n = 6). In the first group, rats
received distilled water (2 mg/kg), in the second, lead acetate (LA) (120 mg/kg), in the third, ascorbic
acid (100 mg/kg), and the 4th, 5th, and 6th groups, rats received LA (120 mg/kg) and EECl (375 mg/kg,
750 mg/kg, and 1500 mg/kg, respectively) for 14 days. Results: A significant learning and memory
deficit was seen in the LA‑treated group’s results, but a significant improvement was seen in the
EECl‑treated group. Increased oxidative stress was seen in the LA‑treated group, as evidenced by
an increase in MDA levels and a decrease in antioxidant enzymes (SOD and GSH). A decline in
MDA levels and an increase in SOD and GSH activity was the evidence of the ameliorative effects of
EECl treatment. Cytoarchitectural distortions relative to the control were observed with the LA‑treated
group. Mild distortion was however detected with EECl treatment. Conclusion: EECl has possible
neurotherapeutic properties against LA‑induced pathological changes in the hippocampus of Wistar
rats. EECl may have neuroprotective effects against degenerative alterations brought on by LA.

Recent years have seen a surge in psychiatric diseases, which has resulted in considerable disease
distress and considerably decreased living conditions. Many considerable synthetic medications have
been used to treat these illnesses throughout the years, but they have been found to have limited
effects and substantial recurrence risks in many individuals. Mental illnesses such as depression
and anxiety are persistently on the rise around the world, posing serious challenges to the affected
person’s and their family members’ personal lives. There is mounting evidence that suggests the gut–
brain axis (GBA) contributes to the genesis and development of psychiatric diseases. This review
focuses on contemporary dietary therapies such as Mediterranean diets and dietary supplements
and emphasizes nutrition’s critical role in psychiatric care through the GBA. Several research have
indicated that dietary quality affects mental health because it controls metabolic processes, has
anti‑inflammatory and antiapoptotic characteristics, and promotes neurogenesis and synaptogenesis.
This study demonstrates many dietary components, their relationships to depression, and how they
work. The use of dietary recommendations to support mental health appears to be a novel, affordable,
useful, nonpharmacological intervention for people with mental problems.

Background: Tramadol has a high potential for misuse resulting in cognitive impairment.
Zingiber officinale, however, possesses neuroprotective qualities. Objective: Microscopically
assessed hippocampal CA1 and CA3 following Z. officinale and tramadol treatment.
Materials and Methods: Two milliliters/kilogram of distilled water was given to Group 1,
Groups 2–5 were administered 50 mg/kg of tramadol while Group 3 was also administered 12.5 mg/
kg of naltrexone, and Groups 4 and 5 were also administered 500, and 1000 mg/kg ethanol extract of
Z. officinale (EEZO), respectively, orally for 21 days. The rats were euthanized and their brains were
collected, fixed in 10% formal saline, and processed routinely using crystal fast violet (CFV) stain for
the demonstration of Nissl substance, glial fibrillary acidic protein (GFAP) for the demonstration of
astrocytes, and Hematoxylin and Eosin for general histoarchitecture and estimation of cell number and
volume using physical dissector and Cavalieri estimator, respectively. Results: CFV stain revealed
alterations in regions of CA1 and CA3 of the hippocampus presenting as indistinct staining intensity
and peripheral Nissl substance accumulation in the tramadol‑treated group. GFAP revealed numerous
reactive astrocyte processes. The area of reactive astrocytes remarkably increased (P < 0.05) and
the intensity of the Nissl substance remarkably reduced in the tramadol-exposed group. When
compared to the control, the tramadol-exposed group’s hippocampal volume considerably (P < 0.05)
decreased (coefficient of error [CE] =0.050). The tramadol treatment group (CE = 0.090) relative to
the control group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal
cells in the CA3 region. The tramadol treatment group (CE = 0.090) compared to the control
group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal cells in the
CA3 region. Tramadol toxicity was attenuated in the groups treated with EEZO in a dose-dependent
manner. Conclusion: Z. officinale possesses a potential neuroprotective effect against tramadol‑induced
neurotoxicity.