Aging is associated with detrimental cellular and cognitive changes, making it an important public health concern; yet, many of these changes may be influenced by nutritional interventions. The natural sesquiterpene β-caryophyllene (BCP) has anti-inflammatory and antioxidant effects that are mediated by cannabinoid type-2 receptor activation, and these actions promote neuroprotection in different animal models that involve a cognitive damage. Consequently, whether chronic administration of BCP might prevent the age-related cellular and cognitive damage in a model of aging induced by chronic d-galactose (GAL) consumption was assessed here. Male BALB/c mice were administered BCP (10 mg/kg, oral), GAL (300 mg/kg, intraperitoneal), or GAL+BCP, and long-term memory and cognitive flexibility were evaluated in the normal and the reverse phases of Morris water maze test. In addition, immunohistochemistry was performed on prefrontal and hippocampal brain slices to detect glial acidic fibrillary protein and DNA oxidation. Although GAL administration reduced cognitive flexibility (P = .0308), this functional damage was not reversed by administering BCP. However, GAL administration also elevated the total number of astrocytes and their interactions in the hippocampus, and increasing DNA oxidation in the prefrontal cortex. BCP administration impeded the rise in the total number of astrocytes (P = .0286) and the DNA oxidation (P = .0286) in mice that received GAL. Hence, although BCP did not improve cognitive flexibility, it did produce a neuroprotective effect at the molecular and cellular level in the GAL model of aging.

中文翻译：

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β-石竹烯减少了d-半乳糖诱导的老年BALB / c小鼠的前额叶皮层和海马中的DNA氧化和胶质原纤维酸性蛋白的过表达。

衰老与有害的细胞和认知变化有关，使其成为重要的公共卫生问题。然而，许多这些变化可能受到营养干预的影响。天然倍半萜烯β-石竹烯（BCP）具有由2型大麻素受体激活介导的抗炎和抗氧化作用，并且这些作用在涉及认知损害的不同动物模型中促进了神经保护作用。因此，BCP的长期给药是否会防止衰老引起的慢性模型与年龄有关的细胞和认知损害d此处评估了半乳糖（GAL）的消耗量。雄性BALB / c小鼠接受BCP（10 mg / kg，口服），GAL（300 mg / kg，腹膜内）或GAL + BCP给药，并在正常和反向阶段评估长期记忆和认知灵活性莫里斯水迷宫测试。此外，对前额叶和海马脑片进行了免疫组织化学，以检测神经胶质酸性原纤维蛋白和DNA氧化。尽管GAL给药会降低认知灵活性（P  = .0308），但BCP不能逆转这种功能损害。但是，GAL给药也增加了海马中星形胶质细胞的总数及其相互作用，并增加了额叶前额叶皮层中的DNA氧化。BCP给药阻止了星形胶质细胞总数的增加（P = .0286）和 接受GAL的小鼠的DNA氧化（P = .0286）。因此，尽管BCP不能改善认知灵活性，但它确实在衰老的GAL模型中在分子和细胞水平上产生了神经保护作用。