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OBJECTIVE: This study aims to investigate the correlation of platelet parameters and C-reactive protein (CRP) with depression. METHODS: The clinical data of 61 patients with depression and 30 healthy control subjects were collected to compare the platelet parameters, CRP levels, and Hamilton Depression Rating Scale (HAMD) scores of the two groups for correlation analysis. RESULTS: The results revealed that the body mass index (BMI) of patients with depression was lower (P < 0.05) than that of the healthy control subjects, and that this difference was more significant in women than in men. Patients with severe depression showed an increased mean platelet volume (MPV) (P < 0.05). In the patients with depression, MPV was positively correlated (P < 0.05) with HAMD scores for work and interest, gastrointestinal symptoms, hopelessness, the anxiety/somatization factor, and the hopelessness factor. Platelet count (PLT) was negatively correlated (P < 0.05) with HAMD scores for hypochondriasis, and plateletcrit (PCT) was negatively correlated (P < 0.05) with HAMD scores for middle insomnia and hypochondriasis. Platelet distribution width (PDW) was positively correlated (P < 0.05) with HAMD scores for gastrointestinal and systemic symptoms as well as hopelessness. Higher CRP levels (P < 0.05) were found in the patients with depression than in the healthy control subjects. Furthermore, in the patients with depression, CRP levels were positively correlated (P < 0.05) with HAMD scores for guilt and the cognitive impairment factor. CONCLUSION: Classical platelet parameters (PLT, MPV, PCT, PDW) and CRP were shown to be associated with specific depressive symptoms and cognitive impairment factors, including sleep, gastrointestinal symptoms, hypochondriasis, losing interest in work, and despair. These results suggest that both platelet parameters and CRP could be suitable biomarkers for predicting the occurrence and prognosis of depression, thus providing a new target for its treatment.
RESUMO
OBJECTIVE: To observe the neural apoptosis and expression of apoptosis-related genes in brain in order to elucidate the regulation mechanism in the perihematomal region of intracerebral hemorrhage (ICH) patients. METHODS: Specimens of perihematomal region in human brain were obtained from 29 patients undergoing surgical evacuation of an intracerebral hematoma. Specimens of brain tissue were collected from the corpses of 6 persons within 3 hours after the accidental death. Neural apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridine 5' triphosphate nick end labeling (TUNEL) method and immunohistochemistry was used to detect the expression of Bcl-2, Bax, P53, and caspase-3 genes. RESULTS: The apoptosis rates of the ICH group was 4.10 +/- 0.28, significantly higher than that of the control group (0.57 +/- 0.43, P < 0.01). The expression rate of Bcl-2 the ICH group was 2.68 +/- 0.52, significantly higher than that of the control group (1.54 +/- 0.56, P < 0.01). The expression rate of Bax of the ICH group was 3.49 +/- 0.18, significantly higher than that of the control group (0.96 +/- 0.27, P < 0.01). The expression of P53 was 4.12 +/- 0.63, significantly higher than that of the control group (0.96 +/- 0.71, P < 0.01). The expression of caspase-3 of the ICH group was 3.50 +/- 0.25, significantly higher than that of the control group (0.74 +/- 0.73, P < 0.01). The expression levels of Bcl-2 and P53 were negatively correlated with the apoptosis rate (both P < 0.01), while the expression levels of Bax and caspase-3, and the Bax/Bcl-2 ratio were positively correlated with the apoptosis rate in perihematomal region of ICH patients (all P < 0.01). CONCLUSION: Apoptosis is involved in the delayed brain injury after ICH in human and is the main factor of delayed neural death. Some of the genes take part in the regulation of neural apoptosis: Bax and caspase-3 hasten the apoptosis while Bcl-2 and P53 restrain it.
