Oral Chinese Herbal Medicine for Depressive Disorder in Patients after Percutaneous Coronary Intervention: A Systematic Review and Meta-Analysis / 中国结合医学杂志

OBJECTIVE@#To evaluate the effectiveness and safety of oral Chinese herbal medicines (CHMs) on post-percutaneous coronary intervention (PCI) patients with depressive disorder in coronary heart disease (CHD).@*METHODS@#A literature search was conducted through databases including PubMed, Cochrane Library, Chinese National Knowledge Infrastructure Databases (CNKI), Chinese Biomedical Literature Database (SinoMed), Chongqing VIP Chinese Science and Technology Periodical Database (VIP) and Wanfang Database up to August 2018. Randomized controlled trials (RCTs) comparing CHMs with placebo or no additional treatments on the basis of standard conventional pharmacological therapies were included. Data extraction, analyses and quality assessment were performed according to the Cochrane standards. RevMan 5.3 software was used to synthesize the results.@*RESULTS@#A total of 16 RCTs enrolling 1,443 participants were included in this systematic review. When compared with antidepressants alone, CHMs showed similar benefits with less side effects [risk ratio=0.54, 95% confidence interval (CI) 0.43 to 0.69, 582 patients]; meanwhile, the combination therapy may have more advantages than antidepressants alone [mean difference (MD)=-1.03, 95%CI-1.81 to-0.25, 267 patients). When identified with placebo, CHMs seem to have more advantages in relieving depressive symptoms (MD=-19.00, 95%CI-20.02 to-17.98, 189 patients). However, when compared with basic treatment of post- PCI, CHMs showed different results in two trials. In terms of post-PCI related clinical symptoms, CHMs seem to have more advantages in relieving chest pain and other general clinical symptoms. However, the heterogeneity in this review was generally high, it may be caused by different interventions used in each trial and the low quality of the trials.@*CONCLUSIONS@#In total, CHMs showed potentially beneficial effects on depressive symptoms and post-PCI related clinical symptoms. However, because of small sample size and potential bias of most trials, this result should be interpreted with caution. More rigorous trials with larger sample size and higher quality are warranted to give high quality of evidence to support the use of CHMs for CHD complicated with depression.

Increased Chondrocyte Apoptosis in Kashin-Beck Disease and Rats Induced by T-2 Toxin and Selenium Deficiency / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease (KBD) and in an established T-2 toxin- and selenium (Se) deficiency-induced rat model.</p><p><b>METHODS</b>Cartilages were collected from the hand phalanges of five patients with KBD and five healthy children. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to T-2 toxin exposure. The apoptotic chondrocytes were observed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Caspase-3, p53, Bcl-2, and Bax proteins in the cartilages were visualized by immunohistochemistry, their protein levels were determined by Western blotting, and mRNA levels were determined by real-time reverse transcription polymerase chain reaction.</p><p><b>RESULTS</b>Increased chondrocyte apoptosis was observed in the cartilages of children with KBD. Increased apoptotic and caspase-3-stained cells were observed in the cartilages of rats fed with normal and Se-deficient diets plus T-2 toxin exposure compared to those in rats fed with normal and Se-deficient diets. Caspase-3, p53, and Bax proteins and mRNA levels were higher, whereas Bcl-2 levels were lower in rats fed with normal or Se-deficiency diets supplemented with T-2 toxin than the corresponding levels in rats fed with normal diet.</p><p><b>CONCLUSION</b>T-2 toxin under a selenium-deficient nutritional status induces chondrocyte death, which emphasizes the role of chondrocyte apoptosis in cartilage damage and progression of KBD.</p>

Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

<p><b>OBJECTIVE</b>To identify the relationship between T-2 toxin and Kashin-Beck disease (KBD), the effects of T-2 toxin on aggrecan metabolism in human chondrocytes and cartilage were investigated in vitro.</p><p><b>METHODS</b>Chondrocytes were isolated from human articular cartilage and cultured in vitro. Hyaluronic acid (HA), soluble CD44 (sCD44), IL-1beta and TNF-alpha levels in supernatants were measured by enzyme-linked immunosorbent assay (ELISA). CD44 content in chondrocyte membrane was determined by flow cytometry (FCM). CD44, hyaluronic acid synthetase-2 (HAS-2) and aggrecanases mRNA levels in chondrocytes were determined using reverse transcription polymerase chain reaction (RT-PCR). Immunocytochemical method was used to investigate expressions of BC-13, 3-B-3(-) and 2-B-6 epitopes in the cartilage reconstructed in vitro.</p><p><b>RESULTS</b>T-2 toxin inhibited CD44, HAS-2, and aggrecan mRNA expressions, but promoted aggrecanase-2 mRNA expression. Meanwhile, CD44 expression was found to be the lowest in the chondrocytes cultured with T-2 toxin and the highest in control plus selenium group. In addition, ELISA results indicated that there were higher sCD44, IL-1beta and TNF-alpha levels in T-2 toxin group. Similarly, higher HA levels were also observed in T-2 toxin group using radioimmunoprecipitation assay (RIPA). Furthermore, using monoclonal antibodies BC-13, 3-B-3 and 2-B-6, strong positive immunostaining was found in the reconstructed cartilage cultured with T-2 toxin, whereas no positive staining or very weak staining was observed in the cartilage cultured without T-2 toxin. Selenium could partly inhibit the effects of T-2 toxin above.</p><p><b>CONCLUSION</b>T-2 toxin could inhibit aggrecan synthesis, promote aggrecanases and pro-inflammatory cytokines production, and consequently induce aggrecan degradation in chondrocytes. These will perturb metabolism balance between aggrecan synthesis and degradation in cartilage, inducing aggrecan loss in the end, which may be the initiation of the cartilage degradation.</p>