Objective: Chronic scrotal hyperthermia (SHT) can lead to serious disorders of the male reproductive system, with oxidative stress playing a key role in the onset of these dysfunctions. Thus, we evaluated the impact of caffeine, a potent antioxidant, on cellular and tissue disorders in mice with chronic SHT. Methods: In this experimental study, 56 adult male NMRI mice were allocated into seven equal groups. Apart from the non-treated control group, all were exposed to heat stress. Two groups, termed “preventive” and “curative,” were orally administered caffeine. The preventive mice began receiving caffeine immediately prior to heat exposure, while for the curative group, a caffeine regimen was initiated 15 consecutive days following cessation of heat exposure. Each treated group was subdivided based on pairing with a positive control (Pre/curative [Cur]+PC) or a vehicle (Pre/Cur+vehicle). Upon conclusion of the study, we assessed sperm characteristics, testosterone levels, stereological parameters, apoptosis, antioxidant and oxidant levels, and molecular markers. Results: Sperm parameters, testosterone levels, stereological parameters, biochemical factors (excluding malondialdehyde [MDA]), and c-kit gene expression were significantly elevated in the preventive and curative groups, especially the former, relative to the other groups. Conversely, expression levels of the heat shock protein 72 (HSP72) and nuclear factor kappa beta (NF-κβ) genes, MDA levels, and apoptotic cell density were markedly lower in both caffeine-treated groups relative to the other groups, with more pronounced differences observed in the preventive group. Conclusion Overall, caffeine attenuated cellular and molecular abnormalities induced by heat stress in the testis, particularly in the mice treated under the preventive condition.

Background: Auraptene is a simple coumarin that exhibits multiple protective activities in the brain. Alzheimer’s disease is a complex, multifactorial, and progressive neurodegenerative disease. Microinjection of the β-amyloid peptide (Aβ) into the hippocampus of rat has been recognized as a reliable and stable animal model of Alzheimer’s disease, which mimics the memory deficits. In the present study, the memory enhancing effects of auraptene were studied in rats that Aβ was injected into their hippocampus to create a model of Alzheimer’s disease. Methods: Different doses of auraptene (5, 10 and 25 mg/kg) were administered intraperitoneally to male Wistar rats. The spatial memory performance was tested by Morris water maze after Alzheimer`s induction. The hippocampal expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins were calculated for evaluating the neuroprotective and anti-apoptotic effects of Auraptene in the brain tissue. Results: In comparison with the control group, auraptene significantly decreased the escape latency time in the treated rats. In addition, auraptene increased the percentage of time spent and traveled pathway in the target quadrant. Molecular data showed that auraptene attenuated the Bax/Bcl-2 ratio in the hippocampus of rats. Conclusion: This study demonstrated the memory enhancing effect of Aur after Aβ injection, which could be through inhibiting the apoptotic pathways in the hippocampus of rats.