Obesity and exposure to fine particulate matter (air pollutant PM_2.5) are important risk factors for metabolic and cardiovascular diseases. They are also related to early menopause. The reduction of 17β-estradiol (E2) levels during female climacteric, marked by menopause, is of significant concern because of its imminent influence on metabolism, redox and inflammatory status. This complex homeostasis-threatening scenario may induce a heat shock response (HSR) in cells, enhancing the expression of the 70 kDa heat shock protein (HSP70). A failure in this mechanism could predispose women to cardiovascular diseases. In this study, we evaluated if the climacteric could represent an additional risk among obese rats exposed to PM_2.5 by worsening lipid, oxidative, and inflammatory parameters and HSP70 in cardiac tissue. We induced obesity in female Wistar rats using a high-fat diet (HFD) (58.3% as fats) and exposed them to 50 μL of saline 0.9% (control, n = 15) or 250 μg residual oil fly ash (ROFA, the inorganic portion of PM_2.5) (polluted, n = 15) by intranasal instillation, 5 days/w for 12 weeks. At the 12th week, we subdivided these animals into four groups: control (n = 6), OVX (n = 9), polluted (n = 6) and polluted + OVX (n = 9). OVX and polluted + OVX were submitted to a bilateral ovariectomy (OVX), a surgical model for menopause, while control and polluted received a false surgery (sham). ROFA exposure and HFD consumption were continued for 12 additional weeks, after which the animals were euthanized. ROFA enhanced the susceptibility to ovariectomy-induced dyslipidemia, while ovariectomy predisposed female rats to the ROFA-induced decrease of cardiac iHSP70 expression. Ovariectomy also decreased the IL-6 levels and IL-6/IL-10 in obese animals, reinforcing a metabolic impairment and a failure to respond to unfavorable conditions. Our results support the hypothesis that obese ovariectomized animals are predisposed to a metabolic worsening under polluted conditions and are at higher risk of cardiovascular diseases.

肥胖和接触细颗粒物（空气污染物PM _2.5）是代谢和心血管疾病的重要危险因素。它们也与更年期早期有关。女性更年期期间以更年期为标志的17β-雌二醇（E2）水平的降低是令人关注的，因为它对代谢，氧化还原和炎症状态的影响迫在眉睫。这种复杂的动态平衡威胁场景可能会诱导细胞产生热休克反应（HSR），从而增强70 kDa热休克蛋白（HSP70）的表达。这种机制的失败可能使妇女容易患心血管疾病。在这项研究中，我们评估了更年期是否可能在暴露于PM _2.5的肥胖大鼠中代表其他风险通过使心脏组织中的脂质，氧化和炎症参数以及HSP70变差。我们使用高脂饮食（HFD）（脂肪为58.3％）诱导雌性Wistar大鼠肥胖，并将其暴露于50μL生理盐水0.9％（对照组，n  = 15）或250μg残留油粉煤灰（ROFA，鼻内滴注，PM _5的无机部分（污染，n = 15），以5天/周的剂量持续12周。在第12周，我们将这些动物分为四组：对照组（n  = 6），OVX（n = 9），污染（n = 6）和污染+ OVX（n = 9）。将OVX和受污染+ OVX提交至更年期手术模型双侧卵巢切除术（OVX），而对照和受污染的则接受了假手术（假手术）。ROFA暴露和HFD消耗再持续12周，然后对动物实施安乐死。ROFA增强了对卵巢切除术引起的血脂异常的敏感性，而卵巢切除术使雌性大鼠易患ROFA诱导的心脏iHSP70表达降低。卵巢切除术还降低了肥胖动物的IL-6水平和IL-6 / IL-10，从而增强了新陈代谢的损害，并且无法应对不利条件。我们的研究结果支持以下假设：肥胖的卵巢切除动物在污染的条件下容易发生代谢恶化，并且罹患心血管疾病的风险更高。