Attenuative effects of collagen peptide from milkfish (Chanos chanos) scales on ovariectomy-induced osteoporosis.

Osteoporosis is characterized by low bone mass, bone microarchitecture disruption, and collagen loss, leading to increased fracture risk. In the current study, collagen peptides were extracted from milkfish scales (MS) to develop potential therapeutic candidates for osteoporosis. MS was used to synthesize a crude extract of fish scales (FS), collagen liquid (COL), and hydroxyapatite powder (HA). COL samples were further categorized according to the peptide size of total COL (0.1 mg/mL), COL < 1 kDa (0.1 mg/mL), COL: 1-10 kDa (0.1 mg/mL), and COL > 10 kDa (0.1 mg/mL) to determine it. Semi-quantitative reverse transcription polymerase chain reaction (sqRT-PCR) and immunofluorescence labeling were used to assess the expression levels of specific mRNA and proteins in vitro. For in vivo studies, mice ovariectomy (OVX)-induced postmenopausal osteoporosis were developed, while the sham surgery (Sham) group was treated as a control. Collagen peptides (CP) from MS inhibited osteoclast differentiation in RAW264.7 cells following an insult with nuclear factor kappa-B ligand (RANKL). CP also enhanced osteoblast proliferation in MG-63 cells, possibly through downregulating NFATc1 and TRAP mRNA expression and upregulating ALP and OPG mRNA levels. Furthermore, COL1 kDa also inhibited bone density loss in osteoporotic mice. Taken together, CP may reduce RANKL-induced osteoclast activity while promoting osteoblast synthesis, and therefore may act as a potential therapeutic agent for the prevention and control of osteoporosis.

Anti-Inflammatory and Chondro-Protective Effects of Acidic Polysaccharide from Enteromorpha Prolifera in Experimental Models of Osteoarthritis In-Vitro and In-Vivo.

OBJECTIVE: Osteoarthritis (OA) progression has been shown to increase the expression of inflammatory cytokines in joints, leading to the destruction of cartilage matrix. Interleukin (IL)-1ß is a potent inflammatory cytokine associated with osteoarthritic synovial fluid. The protective effects of polysaccharides from Enteromorpha prolifera against acute hepatic injury was reported. DESIGN: In this study, we examined the effects of Enteromorpha polysaccharide extracts (EPEs) in the treatment of OA. The effects of the EPEs were assessed using an IL-1ß-stimulated SW1353 and SW982 cells. The expression levels of specific mRNA and proteins were evaluated using semi-quantitative reverse transcription polymerase chain reaction (sqRT-PCR) and western immunoblotting. An OA animal study involving C57BL/6J mice was also conducted to assess the effects on tactile sensitivity and anterior cruciate ligament transection (ACLT). RESULTS: Acidic polysaccharide extract (APE) was shown to significantly reduce cytokine and chemokine mRNA levels in IL-1ß-stimulated SW1353 and SW982 cells and attenuate the expression of proinflammatory cytokines and p38/AP-1 in SW1353 cells. APE was also shown to minimize the effect of osteolytic lesions in the knee joints of ACLT-induced osteoarthritic mice. CONCLUSIONS: APE is a potent inhibitor of joint degeneration associated with OA.

Vascular protection with less activation evoked by progressive thermal preconditioning in adrenergic receptor-mediated hypertension and tachycardia.

Thermal preconditioning may afford cardiovascular protection against oxidative injuries. However, hypertension and taychardia by sympathetic stimulation frequently occur during 420C whole body thermal preconditioning (TP). We aimed to develop a modified TP to achieve cardiovascular protection with to reduced cardiovascular stimulation in the rat. We used a progressive thermal preconditioning (PTP) with three-step 5-min immersion of male Wistar rats in 42 degrees C bath water. Treatment with phentolamine (alpha-adrenergic blocker), propranolol (beta-adrenergic blocker) and atropine (muscarinic cholinergic blocker) was used to evaluate the effect and mechanism of PTP on systemic hemodynamics. Protective function was evaluated by FeCl3-induced acute femoral arterial occlusion (TTO) and heat shock protein 70 expression. Our results show that TP enhanced body temperature, hypertension and tachycardia. However, PTP produced a similar increase in body temperature with significantly less enhancement of hypertension and tachycardia when compared with the TP group. TP- or PTP-induced increase of blood pressure and heart rate was inhibited by phentolamine and propranolol, respectively. PTP-induced attenuation of changes in hemodynamic parameters was via alpha- and beta-adrenergic inhibition. FeCl3 induced femoral arterial injury indicated by TTO at 416 +/- 51 sec in the control rats. After 24 h of TP or PTP treatment with or without adrenergic blocker treatment, TP or PTP upregulated similar femoral arterial heat shock protein 70 expression and significantly (P < 0.05) delayed FeCl3-induced femoral TTO to a similar degree. PTP may provide vascular protection against oxidative injuries with less activation in alpha-adrenergic receptor-mediated hypertension and beta-adrenergic receptor-mediated tachycardia.