ABSTRACT
Objective:To observe the efficacy of self-help cognitive behavioral therapy for insomnia (CBTI), trazodone hydrochloride and their combination in the treatment of depression and insomnia comorbidity in the elderly.Methods:90 elderly patients with insomnia and depression admitted to the 901th Hospital of the Joint Logistic Support Force from October 2019 to October 2021 were selected as the study subjects. They were divided into trazodone group, CBTI group and trazodone combined with CBTI group(combination group), with 30 cases in each group. Trazodone group was treated with oral trazodone hydrochloride, CBTI group was treated with self-help CBTI, and the combination group was treated with oral trazodone hydrochloride combined with self-help CBTI. All three groups were treated for 4 weeks. The sleep latency, total sleep time and sleep efficiency of each group were compared at the time of admission and after 4 weeks of treatment. Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS) were used for sleep assessment before and after treatment, and Self-Rating Depression Scale (SDS) was used for depression assessment.Results:Before treatment, there was no significant difference among the three groups in terms of sleep latency, total sleep time, sleep efficiency, PSQI, ESS and SDS (all P>0.05). After treatment, the sleep latency of the three groups was shorter than that before treatment, and the total sleep time was longer than that before treatment (all P<0.05). The sleep efficiency of the trazodone group and the combination group was higher than that before treatment, with statistically significant difference (both P<0.05). The indexes of the combined group were better than those of the trazodone group and the CBTI group (all P<0.05). The sleep latency of the trazodone group was shorter than that of the CBTI group, and the total sleep time was longer than that of the CBTI group (all P<0.05), with statistically significant difference (all P<0.05). After treatment, the PSQI, except for the SDS of CBTI group, the ESS and SDS of the three groups were lower than those before treatment (all P<0.05). The PSQI, ESS and SDS of the combined group were lower than those of the trazodone group and the CBTI group, and the ESS and SDS of the trazodone group were lower than those of the CBTI group, with statistically significant difference (all P<0.05). Conclusions:For the elderly patients with depression and insomnia, the combination of self-help CBTI and trazodone can not only improve insomnia but also relieve depression symptoms, and the effect is better than that of trazodone and self -help CBTI alone.
ABSTRACT
The beneficial effects of hypoxic preconditioning are abolished in the diabetes. The present study was designed to investigate the protective effects and mechanisms of repeated episodes of whole body hypoxic preconditioning (WBHP) in db/db mice. The protective effects of preconditioning were explored on diabetesinduced vascular dysfunction, cognitive impairment and ischemia-reperfusion (IR)-induced increase in myocardial injury. Sixteen-week old db/db (diabetic) and C57BL/6 (non-diabetic) mice were employed. There was a significant impairment in cognitive function (Morris Water Maze test), endothelial function (acetylcholineinduced relaxation in aortic rings) and a significant increase in IR-induced heart injury (Langendorff apparatus) in db/db mice. WBHP stimulus was given by exposing mice to four alternate cycles of low (8%) and normal air O2 for 10 min each. A single episode of WBHP failed to produce protection; however, two and three episodes of WBHP significantly produced beneficial effects on the heart, brain and blood vessels. There was a significant increase in the levels of brain-derived neurotrophic factor (BDNF) and nitric oxide (NO) in response to 3 episodes of WBHP. Moreover, pretreatment with the BDNF receptor, TrkB antagonist (ANA-12) and NO synthase inhibitor (LNAME) attenuated the protective effects imparted by three episodes of WBHP. These pharmacological agents abolished WBHP-induced restoration of p-GSK-3β/GSK-3β ratio and Nrf2 levels in IR-subjected hearts. It is concluded that repeated episodes of WHBP attenuate cognitive impairment, vascular dysfunction and enhancement in IRinduced myocardial injury in diabetic mice be due to increase in NO and BDNF levels that may eventually activate GSK-3β and Nrf2 signaling pathway to confer protection.
ABSTRACT
The beneficial effects of hypoxic preconditioning are abolished in the diabetes. The present study was designed to investigate the protective effects and mechanisms of repeated episodes of whole body hypoxic preconditioning (WBHP) in db/db mice. The protective effects of preconditioning were explored on diabetesinduced vascular dysfunction, cognitive impairment and ischemia-reperfusion (IR)-induced increase in myocardial injury. Sixteen-week old db/db (diabetic) and C57BL/6 (non-diabetic) mice were employed. There was a significant impairment in cognitive function (Morris Water Maze test), endothelial function (acetylcholineinduced relaxation in aortic rings) and a significant increase in IR-induced heart injury (Langendorff apparatus) in db/db mice. WBHP stimulus was given by exposing mice to four alternate cycles of low (8%) and normal air O2 for 10 min each. A single episode of WBHP failed to produce protection; however, two and three episodes of WBHP significantly produced beneficial effects on the heart, brain and blood vessels. There was a significant increase in the levels of brain-derived neurotrophic factor (BDNF) and nitric oxide (NO) in response to 3 episodes of WBHP. Moreover, pretreatment with the BDNF receptor, TrkB antagonist (ANA-12) and NO synthase inhibitor (LNAME) attenuated the protective effects imparted by three episodes of WBHP. These pharmacological agents abolished WBHP-induced restoration of p-GSK-3β/GSK-3β ratio and Nrf2 levels in IR-subjected hearts. It is concluded that repeated episodes of WHBP attenuate cognitive impairment, vascular dysfunction and enhancement in IRinduced myocardial injury in diabetic mice be due to increase in NO and BDNF levels that may eventually activate GSK-3β and Nrf2 signaling pathway to confer protection.