Objective. To investigate the correlation of CTRP9 with coronary atherosclerosis. Methods. Coronary angiography confirmed CAD in 241 patients (62 received CABG) and non-CAD in 121 (55 received valve replacement). Results. Serum levels of LDL-C, CRP, TNF-α, IL-6, and leptin in CAD patients were significantly higher than those in non-CAD patients (P < 0.05), but APN and CTRP9 were lower (P < 0.05). Serum levels of CTRP9 and APN were negatively related to BMI, HOMA-IR, TNF-α, IL-6, and leptin but positively to HDL-C (P < 0.05) in CAD patients. After adjustment of APN, CTRP9 was still related to the above parameters. Serum CTRP9 was a protective factor of CAD (P < 0.05). When compared with non-CAD patients, leptin mRNA expression increased dramatically, while CTRP9 mRNA expression reduced markedly in epicardial adipose tissue of CAD patients (P < 0.05). The leptin expression and macrophage count in CAD group were significantly higher than in non-CAD group, but CAD patients had a markedly lower CTRP9 expression (P < 0.05). Conclusions. Circulating and coronary CTRP9 plays an important role in the inflammation and coronary atherosclerosis of CAD patients. Serum CTRP9 is an independent protective factor of CAD.

The use of collagen hydrolysates (CHs) as a nutraceutical agent in skin aging has gained increasing attention. Here, the effects of various doses and molecular weights of CH from silver carp skin on photoaging in mice were investigated. The ingestion of CH at 50, 100 and 200 mg per kg body weight led to a dose-dependent increase in the hydroxyproline, hyaluronic acid and moisture contents of the skin, but it had no significant effect on the mice body weight, or on the spleen or thymus index. Furthermore, ingesting CH with lower (LMCH, 200-1000 Da, 65%) and higher molecular weight (HMCH, >1000 Da, 72%) significantly increased the skin components and improved the antioxidative enzyme activities in both serum and skin (p < 0.05); LMCH performed better than HMCH. By contrast, gelatin (>120 kDa) ingestion did not bring a significant change compared to model mice. These results indicated that LMCH exerted a stronger beneficial effect on the skin than did either HMCH and gelatin, which supported the feasibility of using LMCH as a dietary supplement from silver carp skin to combat photoaging.

Oxidative stress is becoming increasingly linked to the pathogenesis of abdominal aortic aneurysms (AAAs). The antioxidant activity of flavonoids has attracted attention for their possible role in the prevention of cardiovascular diseases. The purpose of this study was to determine whether an antioxidant mechanism is involved in the aneurysm formation inhibitory effect afforded by quercetin. Male C57/BL6 mice received quercetin continuously from 2 weeks prior to and 6 weeks following the AAA induction with extraluminal CaCl2. Quercetin treatment decreased AAA incidence and inhibited the reactive oxygen species generation, nitrotyrosine formation and lipid peroxidation production in the aortic tissue during AAA development. In addition, quercetin-treated mice exhibited significantly lower expression of the p47phox subunit of nicotinamide adenine dinucleotide phosphate oxidase and inducible nitric oxide synthase, as well as coordinated downregulation of manganese-superoxide dismutase activities and glutathione peroxidase (GPx)-1 and GPx-3 expression. Quercetin also blunted the expression of c-Jun N-terminal kinase (JNK) and phospho-JNK and, in addition, diminished activation of the activator protein (AP)-1 transcription factor. Gelatin zymography showed that quercetin eliminated matrix metalloproteinase (MMP)-2 and MMP-9 activation during AAA formation. In conclusion, the inhibitory effects of quercetin on oxidative stress and MMP activation, through modulation of JNK/AP-1 signaling, may partly account for its benefit in CaCl2-induced AAA.