Rhodiola is a genus of medicinal plants that originated in Asia and Europe and are used traditionally as adaptogens, antidepressants, and anti-inflammatory remedies. Rhodiola plants are rich in polyphenols, and salidroside and tyrosol are the primary bioactive marker compounds in the standardized extracts of Rhodiola rosea. This review article summarizes the bioactivities, including adaptogenic, antifatigue, antidepressant, antioxidant, anti-inflammatory, antinoception, and anticancer activities, and the modulation of immune function of Rhodiola plants and its two constituents, as well as their potential to prevent cardiovascular, neuronal, liver, and skin disorders.

No abstract

No abstract

In this study, we investigated whether the protective effects of Neonauclea reticulata water extract against ultraviolet B (UVB) irradiation in human skin fibroblast cell cultures (Hs68) are governed by its ability to protect against oxidative stress and expression of matrix metalloproteinases (MMPs). We found that Neonauclea reticulata extract exhibited DPPH scavenging activity and inhibited AAPH-induced haemolysis of erythrocytes in a dose- and time-dependent manner. We also found that pretreatment of fibroblasts with Neonauclea reticulata water extract resulted in markedly lower levels of MMP-1, -3, and -9 expressions. Furthermore, our results indicate that Neonauclea reticulata extract inhibits the expression of MMPs by inhibiting ERK, JNK, and p38 phosphorylation. Our results also demonstrate that treatment with Neonauclea reticulata extract protects against UVB-induced depletion of collagen. In addition, Neonauclea reticulata extract did not have a cytotoxic effect. These findings indicate that the antioxidant activity of Neonauclea reticulata extract resulted in inhibition of MMP-1, -3, and -9 expressions and in increased levels of collagen activity. Our results suggest that Neonauclea reticulata extract can protect against photoaging.

Ultraviolet (UV) irradiation is one of the most important extrinsic factors contributing to skin photodamage. After UV irradiation, a series of signal transductions in the skin will be activated, leading to inflammatory response and photoaged skin. In this study, fisetin, a flavonol that exists in fruits and vegetables, was investigated for its photoprotective effects. The results revealed that 5-25 μM fisetin inhibits cyclooxygenase-2 (COX-2) and matrix metalloproteinase (MMP)-1, MMP-3, MMP-9 expression induced by ultraviolet B (UVB) irradiation in human skin fibroblasts. In addition, fisetin suppressed UVB-induced collagen degradation. With regard to its effect on upper-stream signal transduction, we found that fisetin reduced the expression of ultraviolet (UV)-induced ERK, JNK, and p38 phosphorylation in the mitogen-activated protein kinase (MAP kinase) pathway. Furthermore, fisetin reduced inhibitor κB (IκB) degradation and increased the amount of p65, which is a major subunit of nuclear factor-κB (NF-κB), in cytoplasm. It also suppressed NF-κB translocated to the nucleus and inhibited cAMP response element-binding protein (CREB) Ser-133 phosphorylation level in the phosphoinositide 3-kinase/protein kinase B/CREB (PI3K/AKT/CREB) pathway. Finally, fisetin inhibited UV-induced intracellular reactive oxygen species (ROS), prostaglandin E2 (PGE2), and nitric oxide (NO) generation. The mentioned effects and mechanisms suggest that fisetin can be used in the development of photoprotective agents.

Since the U.S. Congress passed the Dietary Supplement Health and Education Act (DSHEA) in 1994, use of herbal products has been growing rapidly worldwide. To ensure consumer health protection, the quality and safety of herbal plants, particularly those used for dietary supplement preparations, must be determined. To date, toxicological data on the identification of genotoxic and tumorigenic ingredients in many raw herbs and their mechanisms of action are lacking. Thus, identification of carcinogenic components in herbal plants is timely and important. In this review, the issues of quality control and safety evaluation of raw herbs and herbal dietary supplements are discussed. Two examples of tumorigenicity and mechanism of tumor induction are discussed: aristolochic acid and riddelliine, both of which have been detected in Chinese herbal plants. It is proposed that an organized effort with international participation on cancer risk assessment should be actively pursued so that the safety of commercial herbal plants and herbal dietary supplements can be ensured.

In this study, we investigated the antioxidant activity and anti-photoaging properties of an extract of Flemingia macrophylla, a plant rich in isoflavonoid content. Pretreatment of fibroblasts with Flemingia macrophylla extract (FME) inhibited elastase activity, promoted the protein expression of type I procollagen, and attenuated the phosphorylation of mitogen-activated protein (MAP) kinase and the protein expression of matrix-metalloproteinase- (MMP-) 1, 3, and 9. The IC50 values were 2.1 μg/mL for DPPH radical scavenging ability, 366.8 μg/mL for superoxide anion scavenging ability, 178.9 μg/mL for hydrogen peroxide scavenging ability, and 230.9 μg/mL for hydroxyl radical scavenging ability. Also, exposure of erythrocytes to various concentrations of FME (50–500 μg/mL) resulted in a dose- and time-dependent inhibition of AAPH-induced hemolysis. In human fibroblasts, FME at 10 μg/mL was shown to be a potent scavenger of UV-induced reactive oxygen species (ROS). The antioxidant and anti-photoaging properties of FME make it an ideal anti-intrinsic aging and anti-photoaging agent.

This study investigated whether Terminalia catappa L. hydrophilic extract (TCLW) prevents photoaging in human dermal fibroblasts after exposure to UVB radiation. TCLW exhibited DPPH free radical scavenging activity and protected erythrocytes against AAPH-induced hemolysis. In the gelatin digestion assay, the rates of collagenase inhibition by TCL methanol extract, TCLW, and its hydrolysates were greater than 100% at the concentration of 1 mg/mL. We found that serial dilutions of TCLW (10–500 μg/mL) inhibited collagenase activity in a dose-dependent manner (82.3% to 101.0%). However, TCLW did not significantly inhibit elastase activity. In addition, TCLW inhibited MMP-1 and MMP-9 protein expression at a concentration of 25 μg/mL and inhibited MMP-3 protein expression at a concentration of 50 μg/mL. TCLW also promoted the protein expression of type I procollagen. We also found that TCLW attenuated the expression of MMP-1, -3, and -9 by inhibiting the phosphorylation of ERK, JNK, and p38. These findings suggest that TCLW increases the production of type I procollagen by inhibiting the activity of MMP-1, -3 and -9, and, therefore, has potential use in anti-aging cosmetics.