• Journal of Life Science
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• v.25 no.1
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• pp.93-100
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• 2015

Pachymic acid (PA) is a lanostane-type triterpenoid derived from the Poria cocos mushroom. Several beneficial biological features of PA provide medicine with a wide variety of valuable effects, such as anticancer and anti-inflammatory activity; it also has antioxidant effects against oxidative stress. Nonetheless, the biological properties and mechanisms that produce this anti-cancer action of PA remain largely undetermined. In this study, we investigated the pro-apoptotic effects of PA in T24 human bladder cancer cells. It was found that PA could inhibit the cell growth of T24 cells in a dose-dependent manner, which was associated with the induction of apoptotic cell death, as evidenced by the formation of apoptotic bodies and chromatin condensation and accumulation of cells in the sub-G1 phase. The induction of apoptotic cell death by PA was connected with an up-regulation of pro-apoptotic Bax and Bad protein expression and down-regulation of anti-apoptotic Bcl-2 and Bcl-xL proteins, and inhibition of apoptosis family proteins. In addition, apoptosis-inducing concentrations of PA induced the activation of caspase-9, an initiator caspase of the mitochondrial-mediated intrinsic pathway, and caspase-3, accompanied by proteolytic degradation of poly (ADP-ribose)-polymerase. PA also induced apoptosis via a death receptor-mediated extrinsic pathway by caspase-8 activation, resulting in the truncation of Bid and suggesting the existence of cross-talk between the extrinsic and intrinsic pathways. Taken together, the present results suggest that PA may be a potential chemotherapeutic agent for the control of human bladder cancer cells.

• IMMUNE NETWORK
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• v.22 no.4
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• pp.34.1-34.19
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• 2022

Osteoarthritis (OA) is the most common form of arthritis associated with ageing. Vitamin D has diverse biological effect on bone and cartilage, and observational studies have suggested it potential benefit in OA progression and inflammation process. However, the effect of vitamin D on OA is still contradictory. Here, we investigated the therapeutic potential of vitamin D in OA. Six-week-old male Wistar rats were injected with monosodium iodoacetate (MIA) to induce OA. Pain severity, cartilage destruction, and inflammation were measured in MIA-induced OA rats. Autophagy activity and mitochondrial function were also measured. Vitamin-D (1,25(OH)₂D3) and celecoxib were used to treat MIA-induced OA rats and OA chondrocytes. Oral supplementation of vitamin D resulted in significant attenuations in OA pain, inflammation, and cartilage destruction. Interestingly, the expressions of MMP-13, IL-1β, and MCP-1 in synovial tissues were remarkably attenuated by vitamin D treatment, suggesting its potential to attenuate synovitis in OA. Vitamin D treatment in OA chondrocytes resulted in autophagy induction in human OA chondrocytes and increased expression of TFEB, but not LC3B, caspase-1 and -3, in inflamed synovium. Vitamin D and celecoxib showed a synergistic effect on antinociceptive and chondroprotective properties in vivo. Vitamin D showed the chondroprotective and antinociceptive property in OA rats. Autophagy induction by vitamin D treatment may be a promising treatment strategy in OA patients especially presenting vitamin D deficiency. Autophagy promoting strategy may attenuate OA progression through protecting cells from damage and inflammatory cell death.

• Journal of the Korean Society of Food Science and Nutrition
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• v.37 no.9
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• pp.1136-1141
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• 2008

This study was to investigate antiwrinkle effect of mugwort (Artemisia vulgaris) methanol extract in hairless mouse skin induced by UVB-irradiation. Hairless mouse were topically treated with the basic lotion alone (control), ascorbic acid (AA-0.5%, AA-1.0%, AA-2.0%, and AA-5.0%) and mugwort extract (ME-0.5%, ME-1.0%, ME-2.0%, and ME-5.0%) dissolved in a basic lotion. After topical treatment of 30 minutes, the animals were irradiated with increasing doses of UVB radiation ($60{\sim}100\;mJ/cm^2$) for 4 weeks. In our experimental condition, skin thickness of hairless mouse was significantly decreased ($12.5{\sim}21.4%$) in all ME groups compared with control group. Ra value, that is surface roughness parameter induced by skin wrinkling, was significantly decreased ($23.7{\sim}31.1%$) in ME-1.0%, 2.0% and 5.0% group compared with control group. Furthermore, Rq, Rz and Rt value were significantly decreased to $11.2{\sim}21.2%$, $19.8%{\sim}24.5%$, and $14.2%{\sim}22.7%$, respectively. Wrinkle formation of ascorbic acid treatment group as reference group was inhibited, but its effect was less than ME treatment. Matrix metalloproteinase-1 activity was significantly inhibited ($19.7{\sim}22.6%$) compared with control group and collagen content was significantly increased (about 10%) when compared with control group. These results indicate that ME could protect skin aging and wrinkle formation in hairless mouse from photo-irradiation.