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Background/Purpose: Myocarditis is a severe disorder characterized by the inflammation of the heart's muscular walls, thereby leading to sudden death in young adults. Long non-coding RNA X-inactive specific transcripts (LncRNA XIST) are a class of transcripts having a length ˃ 200 nts with the absence of protein-coding abilities. They exert their function of apoptosis in various cancers and inflammatory diseases. background: Myocarditis is a severe disorder characterized by the inflammation of the heart muscular walls leading to the sudden death in young adults. Long non-coding RNA X-inacitve specific transcript (LncRNA XIST) are a class of transcripts having length ˃ 200 nts with absence of protein coding abilities. They exerts its function in apoptosis in various cancers and inflammation diseases. Objective: The current work intended to investigate the impact and mechanism of XIST on inflammation induced by LPS in AC16 cells. objective: The current work intended to investigate the impact and mechanism of XIST in in the inflammation induced by LPS in AC16 cells. Methods: An in vitro inflammatory injury model was established by stimulating AC16 cells with LPS. CCK-8 was used to test AC16 cell viability and FCM to detect apoptosis. The Elisa assay was used to measure the level of IL-8, IL-1β, and TNF-α. The RT-qPCR was used to detect XIST, miR-370-3p, Bax, and Bcl-2 in LPS-stimulated AC16 cells. The Elisa assay was performed to assess the phosphorylation of PI3K, AKT and mTOR in AC16 cells. method: An in vitro inflammatory injury model was established by stimulating AC16 cells with LPS. CCK-8 assay was employed to examine the AC16 cell viability while the cell apoptosis was detected by FCM assay. The level of IL-8, IL-1β, and TNF-α were assessed using Elisa assay. The expression of XIST, miR-370-3p and the mRNA expressions of Bax and Bcl-2 in AC16 cells stimulated with LPS were detected using RT-qPCR. Elisa assay was performed to assess the phosphorylation of PI3K, AKT and mTOR in AC16 cells. Results: Our findings showed LPS exposure to significantly reduce AC16 cell viability while increasing inflammation and apoptosis. Also, XIST expression was reduced in AC16 cells stimulated with LPS. Overexpression of XIST in AC16 cells increased cell survival, inhibited apoptosis, and increased the expressions of Bcl-2, Bax, and inflammatory modulators (IL-8, TNF-α, and IL-1β). Inhibiting XIST in AC16 cells produced opposite outcomes. MiR-370-3p mimics inhibited XIST's effect on inflammation, viability, and apoptosis. Moreover, XIST inhibited the phosphorylation levels of mTOR, AKT, and PI3K in LPS-injured AC16 cells. result: Our results indicated that exposure of LPS significantly decreased the AC16 cell viability while increased the inflammation and apoptosis in AC16 cells. Also, XIST expression was reduced in AC16 cells stimulated with LPS. Overexpression of XIST mitigated the injury induced by LPS in AC16 cells, proved by enhancing the cell viability, inhibiting apoptosis rate and levels of Bcl-2 and Bax and inflammatory modulators (IL-8, TNF-α, and IL-1β) in LPS-stimulated AC16 cells. Besides, opposite results were observed by the inhibition of XIST in AC16 cells. Furthermore, XIST negatively regulated miR-370-3p expression and the impact of XIST overexpression on the inflammation, viability and apoptosis was blocked by miR-370-3p mimic. Moreover, XIST inhibited the phosphorylation level of mTOR, AKT, and PI3K in LPS-injured AC16 cells. Conclusion: The data elucidate lncRNA XIST to exert its anti-inflammatory and anti-apoptotic effects on AC16 cells stimulated by LPS via down-regulating miR-370-3p and inhibiting PI3K/AKT/mTOR pathways. These findings suggest a novel treatment strategy for myocarditis. other: Not applicable

As part of our search for new cytotoxic and antimicrobial natural products from endolichenic fungi, 19 compounds including 1 new 10-member lactone (2), 1 new polyacetylene glycoside (3), 1 new brasilane-type sesquiterpenoid glycoside (4), and 2 isobenzofuran-1(3H)-one derivatives (5 and 6) were isolated from the solid culture of the endolichenic fungus Hypoxylon fuscum. Their structures were unambiguously elucidated by NMR spectroscopic data, MS, ECD (electronic circular dichroism) calculation, and chemical methods. The cytotoxic effects on K562, SW480, and HEPG2 cell lines and the antimicrobial activity against Bacillus subtilis, Staphylococcus aureus, Escherichia coli, and Candida albicans were assessed. Compounds 1, 2, and 5 exhibited moderate cytotoxicity against K562, SW480, and HEPG2 cell lines while compounds 1, 9, and 11 displayed weak antibacterial activity against S. aureus.

Two new arborinane-type triterpenes, myrotheols A (1) and B (2), two new arborinane-type glycosides, myrothesides C (3) and D (4), together with four known diterpenes (5 – 8) were isolated from the ethyl acetate extract of the endolichenic fungus Myrothecium inundatum. The structures of new compounds 1 – 4 were elucidated by NMR and MS analyses. The absolute configuration of 1 was assigned by a single-crystal X-ray diffraction experiment. Compounds 3 and 4 represent the first two natural 4-O-methyl-α-D-mannosides. Compounds 1 – 8 exhibited cytotoxicity against K562 and RKO human cancer cell lines.

Curcumin, which is the effective component of turmeric (Curcuma longa), has previously been shown to exert potent antioxidant, antitumor and anti‑inflammatory activities in vitro and in vivo. However, the mechanism underlying the protective effects of curcumin against oxidative damage in endothelial cells remains unclear. The present study aimed to examine the effects of curcumin on hydrogen peroxide (H2O2)‑induced apoptosis and autophagy in EA.hy926 cells, and to determine the underlying molecular mechanism. Cultured EA.hy926 cells were treated with curcumin (5‑20 µmol/l) 4 h prior to and for 4 h during exposure to H2O2 (200 µmol/l). Oxidative stress resulted in a significant increase in the rate of cell apoptosis, which was accompanied by an increase in the expression levels of caspase‑3 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), and a decrease in the expression levels of Bcl‑2. Treatment with curcumin (5 or 20 µmol/l) significantly inhibited apoptosis, and reversed the alterations in caspase‑3, Bcl‑2 and Bax expression. Furthermore, curcumin induced autophagy and microtubule‑associated protein 1A/1B‑light chain 3‑Ⅱ expression, and suppressed the phosphorylation of Akt and mammalian target of rapamycin (mTOR). These results indicated that curcumin may protect cells against oxidative stress‑induced damage through inhibiting apoptosis and inducing autophagy via the Akt/mTOR pathway.

Five coticolous lichen samples were collected from western Hubei Province of China to analyze the long chain n-alkanes and their carbon isotope compositions. The n-alkanes range in carbon number from C17 to C33 with strong odd-over-even predominance between C21 and C33. Lichens are dominated by n-C29 in the samples of Dajiuhu, Shennongjia Mountain, but by both n-C23 and n- C29 at Qizimei Mountain. This difference may result from the different environmental conditions in these two sites. The δ 13 C values of long chain n-alkanes in lichen samples show the signature of C3 plants. Based on compound- specific carbon isotopic values and previous results, we state that alkane homologs>C23 mainly originate from the symbiotic fungi, while symbiotic algae only contribute trace amount of long chain alkanes. Of great interesting is the occurrence of long chain 3-methylalkanes in the Qizimei samples. These anteiso compounds range from C24 to C32, displaying obvious even-over-odd predomi- nance. This study reveals that the association of long chain 3-methylalkanes with n-C23 alkane might be used as proxies to reconstruct the paleoecological implications of lichens in Earth history.

p27(kip1) (p27) is widely known as a potent cell cycle inhibitor in several organs, especially in the heart. However, its role has not been fully defined during the early phase of myocardial infarction (MI). In this study, we investigated the relationships between p27, vascular endothelial growth factor/hepatocyte growth factor (VEGF/HGF) and NF-κB in post-MI cardiac function repair both in vivo and in the hypoxia/ischemia-induced rat myocardiocyte model. In vivo, haplo-insufficiency of p27 improved cardiac function, diminished the infarct zone, protected myocardiocytes and increased angiogenesis by enhancing the production of VEGF/HGF. In vitro, the presence of conditioned medium from hypoxia/ischemia-induced p27 knockdown myocardiocytes reduced the injury caused by hypoxia/ischemia in myocardiocytes, and this effect was reversed by VEGF/HGF neutralizing antibodies, consistent with the cardioprotection being due to VEGF/HGF secretion. We also observed that p27 bound to IKK and that p27 haplo-insufficiency promoted IKK/p65 activation both in vivo and in vitro, thereby inducing the NF-κB downstream regulator, VEGF/HGF. Furthermore, IKKi and IKK inhibitor negated the effect of VEGF/HGF. Therefore, we conclude that p27 haplo-insufficiency protects against heart injury by VEGF/HGF mediated cardioprotection and increased angiogenesis through promoting IKK activation.