Although astragaloside IV, a saponin isolated from Astragalus membranaceus, has been shown to protect the myocardium against ischemia/reperfusion injury, its effect on the status of sarcoplasmic reticulum (SR) Ca²⁺ transport in the injured myocardium remains largely unknown. In this study, we investigated whether in cultured cardiomyocytes subjected to hypoxia and reoxygenation (H/R) administration of astragaloside IV during H/R attenuates the myocardial cell injury and prevents changes in Ca²⁺ handling activities and gene expression of SR Ca²⁺ pump. Cultured cardiomyocytes from neonatal rats were exposed to 6 h of hypoxia followed by 3 h of reoxygenation. Myocyte injury was determined by the release of cardiac troponin I in supernatant. Astragaloside IV significantly inhibited cardiac troponin I release after H/R in a dose-dependent manner. The diastolic [Ca²⁺]_i measured with Fura-2/AM was significantly increased after reoxygenation. Astragaloside IV prevented the rise of diastolic [Ca²⁺]_i and the depression of caffeine-induced Ca²⁺ transients caused by H/R. Furthermore, the observed depressions in SR Ca²⁺-ATPase activity as well as the mRNA and protein expression of SR Ca²⁺-ATPase in hypoxic-reoxygenated cardiomyocytes were attenuated by astragaloside IV treatment. These results suggest that the beneficial effect of astragaloside IV in H/R-induced injury may be related to normalization of SR Ca²⁺ pump expression and, thus, may prevent the depression in SR Ca²⁺ handling.

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Osteoarthritis (OA) is characterized by a loss of articular cartilage accompanied with inflammation of synovium. β-Ecdysterone (Ecd), a major component of several Chinese herbal medicines, e.g., Achyranthes bidentata BL., has been used for the prevention and treatment of OA. Ecd is an estrogen analog and is likely to have similar pharmacological effects including the effect of protective chondrocytes. This study investigated the effects of Ecd on interleukin-1β (IL-1β)-induced apoptosis and inflammation in rat chondrocytes. Ecd protected chondrocytes from IL-1β-induced injury by inhibiting expression of Bax, p53 phosphorylation, and promoting expression of Bcl-xL . Simultaneously, Ecd reduced caspase 3 activity. IL-1β-induced inflammation and matrix degration were also prevented by Ecd via down-regulation of matrix metalloproteinases MMP 3, MMP 9, and cyclooxygenase-2 expression. Additionally, Ecd inhibited Nuclear Factor Kappa B (NF-κB) p65 phosphorylation, IκBα degradation, and phosphorylation in IL-1β-induced rat chondrocytes. These results suggested Ecd exerted anti-apoptosis and anti-inflammation in IL-1β-induced rat chondrocytes, which might be related to NF-κB signal pathway.

Saponins, an important group of bioactive plant natural products, are glycosides of triterpenoid or steroidal aglycones. Their diverse biological activities are ascribed to their different structures. Saponins have long been recognized as key ingredients in traditional Chinese medicine. Accumulated evidence suggests that saponins have significant neuroprotective effects on attenuation of central nervous system disorders, such as stroke, Alzheimer's disease, Parkinson's disease, and Huntington's disease. However, our understanding of the mechanisms underlying the observed effects remains incomplete. Based on recently reported data from basic and clinical studies, this review highlights the proposed mechanisms of their neuroprotective function including antioxidant, modulation of neurotransmitters, anti-apoptosis, anti-inflammation, attenuating Ca(2+) influx, modulating neurotrophic factors, inhibiting tau phosphorylation, and regeneration of neural networks.