Traditional Chinese medicine (TCM) has been practiced in the treatment of bone diseases and alcoholism. Chronic excessive alcohol use results in alcohol-induced bone diseases, including osteopenia and osteoporosis, which increases fracture risk, deficient bone repair, and osteonecrosis. This preclinical study investigated the therapeutic effects of TCM herbal extracts in animal models of chronic excessive alcohol consumption-induced osteopenia. TCM herbal extracts (Jing extracts) were prepared from nine Chinese herbal medicines, a combinative herbal formula for antifatigue and immune regulation, including Astragalus, Cistanche deserticola, Dioscorea polystachya, Lycium barbarum, Epimedium, Cinnamomum cassia, Syzygium aromaticum, Angelica sinensis, and Curculigo orchioides. In this study, Balb/c male mice were orally administrated alcohol (3.2 g/kg/day) with/without TCM herbal extracts (0.125 g/kg, 0.25 g/kg, or 0.5 g/kg) by gavage. Our results showed that after 50 days of oral administration, TCM herbal extracts prevented alcohol-induced osteopenia demonstrated by μ-CT bone morphological analysis in young adults and middle-aged/old Balb/c male mice. Biochemical analysis demonstrated that chronic alcohol consumption inhibits bone formation and has a neutral impact on bone resorption, suggesting that TCM herbal extracts (Jing extracts) mitigate the alcohol-induced abnormal bone metabolism in middle-aged/old male mice. Protocatechuic acid, a natural phenolic acid in Jing extracts, mitigates in vivo alcohol-induced decline of alkaline phosphatase (ALP) gene expression in the bone marrow of Balb/c male mice and in vitro ALP activity in pre-osteoblast MC3T3-E1 cells. Our study suggests that TCM herbal extracts prevent chronic excessive alcohol consumption-induced osteopenia in male mice, implying that traditional medicinal plants have the therapeutic potential of preventing alcohol-induced bone diseases.

The atmospheric particulate matter with a diameter less than or equal to 2.5 um (PM2.5) can result in increased immune system damage or diseases, however, the possible mechanism remains unclear. In this study, we used Jurkat T cells to determine the effects of PM2.5 on T cell-mediated adaptive immune response. Our results indicated that PM2.5 exposure increased intracellular calcium ion concentration [Ca(2+)]. In contrast, cytosolic free Ca(2+) concentration [Ca(2+)]i significantly decreased in Jurkat T cells transfected with Orai1siRNA. In addition, we detected the level of interleukin (IL)-2 and tumor-necrosis factor (TNF)-α as well as other signalling molecules, including calcineurin (CaN) and NFATc2, a gene on 20q13.2 that encodes a member of the nuclear factor of activated T cells (NFAT), in the supernatant of cells exposed to PM2.5. The expression of NFATc2 protein increased in a time-dependent manner after exposure to PM2.5, but the activity of CaN decreased. NFATc2 was not consistent with IL-2 accumulation, thus indicating the involvement of other signals in the suppression of IL-2 accumulation. Our findings demonstrate that PM2.5 exposure in immune cells results in locally increased [Ca(2+)]i generated by Orai1 and CaN-NFAT gene expression, TNF-α and IL-2 cytoplasmic concentrations may be altered.

Traffic-related PM 2.5 can result in immune system damage and diseases; however, the possible mechanism of its effect remains unclear. Calcium (Ca 2þ) is a critical signaling molecule in a variety of cells. Indeed, Ca 2þ is involved in numerous basic functions, including cell growth and death. In this study, Jurkat T cells were used to explore the possible mechanisms of PM 2.5-elicited intracellular Ca 2þ signal responses. The results indicate that PM 2.5 could raise the level of intracellular Ca 2þ concentration ([Ca 2þ ]i). The [Ca 2þ ]i in Jurkat T cells significantly decreased after treatment with heparin as an inhibitor of inositol trisphosphate receptors (IP3 R), or procaine as an inhibitor of ryanodine receptors (RyR). The expression of calmodulin (CAM) protein decreased in a time-dependent manner after exposure to PM 2.5 , whereas the activity of Ca 2þ-Mg 2þ-ATPase seemed to show a slight drop trend after exposure to PM 2.5. Our findings demonstrate that PM 2.5 stimulation to Jurkat T cells would result in an increase in [Ca 2þ ]i, which is modulated by IP3 R and RyR, as well as CAM.

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Tartary buckwheat is used as an ingredient in flour and tea, as well as in traditional Chinese medicine for its antioxidant effects. Here, we found that an ethanol extract of tartary buckwheat (TBE) potently induced autophagy flux in HeLa cells by suppressing mTORC1 activity, as revealed by dephosphorylation of the mTORC1 substrates Ulk1, S6K, and 4EBP, as well as by the nuclear translocation of transcriptional factor EB. In addition to non-selective bulk autophagy, TBE also induced aggrephagy, which is defined as autophagy against aggregated proteins. Quercetin is a flavonol found at high levels in TBE. We showed that quercetin induced both non-selective bulk autophagy and aggrephagy. These effects were also observed in Huh-7 cells derived from hepatocytes. Thus, aggrephagy induction by TBE and quercetin may relieve alcoholic hepatitis, which is closely linked to the accumulation of protein aggregations called Mallory–Denk bodies.