Hammad Alaa M, Alzaghari Lujain F, Alfaraj Malek, Al-Qerem Walid, Talib Wamidh H, Alasmari Fawaz, Amawi Haneen, Hall F Scott
Department of Pharmacy, College of Pharmacy, Al-Zaytoonah University of Jordan, Amman, Jordan.
Department of Clinical Pharmacy and Therapeutic, Applied Science Private University, Amman, Jordan.
Front Pharmacol. 2023 Jan 9;13:1047236. doi: 10.3389/fphar.2022.1047236. eCollection 2022.
Chronic exposure to cigarette smoke produces neuroinflammation and long-term changes in neurotransmitter systems, especially glutamatergic systems. We examined the effects of cigarette smoke on astroglial glutamate transporters as well as NF-κB expression in mesocorticolimbic brain regions, prefrontal cortex (PFC) and nucleus accumbens (NAc). The behavioral consequences of cigarette smoke exposure were assessed using open field (OF) and light/dark (LD) tests to assess withdrawal-induced anxiety-like behavior. Sprague-Dawley rats were randomly assigned to five experimental groups: a control group exposed only to standard room air, a cigarette smoke exposed group treated with saline vehicle, two cigarette smoke exposed groups treated with acetylsalicylic acid (ASA) (15 mg/kg and 30 mg/kg, respectively), and a group treated only with ASA (30 mg/kg). Cigarette smoke exposure was performed for 2 h/day, 5 days/week, for 31 days. Behavioral tests were conducted weekly, 24 h after cigarette smoke exposure, during acute withdrawal. At the end of week 4, rats were given either saline or ASA 45 min before cigarette exposure for 11 days. Cigarette smoke increased withdrawal-induced anxiety, and 30 mg/kg ASA attenuated this effect. Cigarette smoke exposure increased the relative mRNA and protein expression of nuclear factor ĸB (NFĸB) in PFC and NAc, and ASA treatment reversed this effect. Also, cigarette smoke decreased the relative mRNA and protein expression of glutamate transporter1 (GLT-1) and the cystine-glutamate transporter (xCT) in the PFC and the NAc, while ASA treatment normalized their expression. Cigarette smoke caused neuroinflammation, alterations in glutamate transporter expression, and increased anxiety-like behavior, and these effects were attenuated by acetylsalicylic acid treatment.
长期接触香烟烟雾会导致神经炎症以及神经递质系统的长期变化，尤其是谷氨酸能系统。我们研究了香烟烟雾对中脑边缘脑区、前额叶皮质（PFC）和伏隔核（NAc）中星形胶质细胞谷氨酸转运体以及核因子κB（NF-κB）表达的影响。使用旷场试验（OF）和明暗试验（LD）评估香烟烟雾暴露的行为后果，以评估戒断诱导的焦虑样行为。将Sprague-Dawley大鼠随机分为五个实验组：仅暴露于标准室内空气的对照组、用生理盐水载体处理的香烟烟雾暴露组、用乙酰水杨酸（ASA）（分别为15 mg/kg和30 mg/kg）处理的两个香烟烟雾暴露组，以及仅用ASA（30 mg/kg）处理的组。每天进行2小时、每周5天、持续31天的香烟烟雾暴露。在急性戒断期间每周进行一次行为测试，在香烟烟雾暴露后24小时进行。在第4周结束时，在香烟暴露前45分钟给大鼠注射生理盐水或ASA，持续11天。香烟烟雾增加了戒断诱导的焦虑，30 mg/kg的ASA减弱了这种作用。香烟烟雾暴露增加了PFC和NAc中核因子κB（NFκB）的相对mRNA和蛋白质表达，而ASA处理逆转了这种作用。此外，香烟烟雾降低了PFC和NAc中谷氨酸转运体1（GLT-1）和胱氨酸-谷氨酸转运体（xCT）的相对mRNA和蛋白质表达，而ASA处理使其表达恢复正常。香烟烟雾导致神经炎症、谷氨酸转运体表达改变，并增加焦虑样行为，而乙酰水杨酸处理减弱了这些作用。
