Background: Chemotherapy drugs may lead to hepatic injury, which is considered one of the limitations of these drugs.Objectives: The aim of this study was to evaluate the effect of quercetin (QUE) on M1/M2 macrophage polarization and hepatoprotective effect in cyclophosphamide (CTX)‐induced liver toxicity.Methods: Twenty‐four mice were divided into four groups (Control, QUE, CTX, CTX + QUE). The CTX and CTX + QUE groups received 200 mg/kg CTX. The animals in the QUE and CTX + QUE groups received 50 mg/kg QUE. All animals were sacrificed, and serum and liver samples were used for laboratory analyses.Results: Examinations indicated that CTX exposure led to disruption of liver functions and morphological degenerations. Tissue pro‐apoptotic Bax and caspase 3, pro‐inflammatory TNF‐α and IL‐1β, transcription factor NF‐κB, and M1 macrophage polarization marker CD86 were upregulated significant (p < 0.05) in this group. In addition, CTX exposure led to significantly (p < 0.05) upregulation of the Bax/Bcl‐2 mRNA ratio and DNA fragmentations. The PCNA‐positive hepatic cell ratio and anti‐apoptotic Bcl‐2 expression are remarkably suppressed (p < 0.05). Immunohistochemical analyses are also indicated that M2 macrophage polarization marker CD163 is slightly but remarkably (p < 0.05) downregulated in the CTX group compared to the Control and QUE groups. The morphological and biochemical disruptions were alleviated in QUE‐treated animals in the CTX + QUE group. Liver function test results, apoptosis, inflammatory, transcription factor NF‐κB, regeneration/proliferation, and apoptotic index results in this group were similar (p > 0.05) to the control and QUE groups. The M1 cell surface marker expression of CD86 is significantly (p < 0.05) downregulated, and M2 macrophage polarization marker expression of CD163 is upregulated significantly (p < 0.05) compared to the CTX group.Conclusions: This study indicates that QUE has the potential to downregulate CTX‐induced hepatic injury and regulate M1/M2 macrophage polarization to the M2 side, which indirectly demonstrates activation of anti‐inflammatory signalling and tissue repair.

Effects of Sublethal Doses of Thiacloprid, a Neonicotinoid Insecticide, on Learning and Memory Performance of Mice

Protective Effects of Trolox on Ketamine-Induced Memory Impairments and Morphological Changes in the Brain

Background: Neurosecretory cells of insects synthesize Adipokinetic Hormone (AKH). Previous studies indicated that AKH improves memory functions. Objective: This study aimed to explore the effects of AKH on learning and memory in an Alzheimer's disease model. Methods: Morris Water Maze (MWM), Passive Avoidance (PA), and Modified Elevated Plus Maze (mEPM) tests were conducted in BALB/c mice. Initially, each group consisted of 8 to 9 animals; in total, 120 animals were used in this study. The groups included control, Ani-AKH (1 and 2 mg/kg), Lia-AKH (1 and 2 mg/kg), Pht-HrTH (1 and 2 mg/kg), Scopolamine (1 mg/kg), and Scopolamine combinations. Hormones were given for 6 days in the MWM test to evaluate learning and memory before the second trial in the PA test for memory assessment and after the first trial in the mEPM test to examine consolidation. Results: In the MWM test, Ani-AKH and Pht-HrTH reduced escape latency compared to the scopolamine group (p<0.05). During the probe trial, Ani-AKH increased time in the escape platform quadrant (p<.0.5) and reversed scopolamine's effects (p<0.001). Lia-AKH and Pht-HrTh did not affect time in the quadrant but reversed scopolamine's effects (p<0.01). In the PA test, Ani- AKH reversed scopolamine’s effects (p<.0.5), while Lia-AKH did so in the mEPM test (p<0.01). The control group showed strong muscarinic receptor staining, while the scopolamine group did not. Ani-AKH and Lia-AKH showed moderate to strong receptor staining, indicating partial restoration. Conclusion: Our study indicates that AKH may help reduce memory impairments, though the effects depend on the specific assessment methods used in the tests.