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Chukrasia tabularis is an economically important tree and widely cultured in the southeast of China. Its barks, leaves, and fruits are consumed as a traditional medicine and perceived as a valuable source for bioactive limonin compounds. The extracts from root barks of C. tabularis showed significant anti‐inflammatory effect. The aim of this research was to explore the material basis of C. tabularis anti‐inflammatory activity, and to purify and identify anti‐inflammatory active ingredients. By a bioassay‐guided isolation of dichloromethane fraction obtained two novel phragmalin limonins, Chukrasitin D and E (1 and 2), together with 12 known limonins (3–14). The chemical structure of these compounds is determined on the basis of extensive spectral analysis and chemical reactivity. In addition, the activities of these isolated limonins on the production of nitric oxide (NO), tumor necrosis factor alpha (TNF‐α), and nuclear factor kappa B (NF‐κB) in RAW264.7 cells induced by lipopolysaccharide (LPS) were evaluated. Limonins 1 and 2 indicated significant anti‐inflammatory activity with IC50 values of 6.24 and 6.13 μM. Compound 1 notably inhibited the production of NF‐κB, TNF‐α and interleukin 6 (IL‐6) in macrophages. The present results suggest that the root barks of C. tabularis exhibited anti‐inflammatory effect and the limonins may be responsible for this activity. [ABSTRACT FROM AUTHOR]

One new 14-membered ring cyclopeptide alkaloid, plenane A (1), along with six known compounds (2-7), was isolated from the roots of Clematis florida. Their structures were elucidated by means of NMR spectroscopic analysis and mass spectrometry. In addition, their anti- inflammatory effects on lipopolysaccharide-induced RAW264.7 macrophages were evaluated in vitro. The compounds 1, 2 and 6 exhibited potent indirect inhibitory effects, with IC50 values of 40.92, 22.88 and 6.32 μM, respectively. [ABSTRACT FROM AUTHOR]

Three new phomalone derivatives, phomalichenones E-G (1–3), and seven known analogues (4–10) were isolated from the cultures of a deep-sea-derived fungus Alternaria sp. MCCC 3A00467. Their structures were elucidated by spectroscopic methods, including the 1D and 2D NMR, and ECD spectrum. Among the compounds isolated, phomalichenone F (2) presented cytotoxic activity against human myeloma cancer U266 cells with IC50 value of 24.99 μg/mL. The most active compound, 10, showed cytotoxicity against U266, HepG2 and A549 cells with IC50 values of 13.26, 14.69 and 24.39 μg/mL, respectively. [ABSTRACT FROM AUTHOR]

Clematis florida is widely used in She Ethnopharmacy in China owing to its significant anti-inflammatory activities. This study aimed to investigate the anti-inflammatory effect of the active fraction of C. florida (CFAF) in an arthritis animal model and its possible mechanism. Pre-inflammatory cytokine levels were examined by ELISA. CFAF can significantly improve the symptoms of arthritis such as paw swelling, arthritic index, and histological condition in AA rat. CFAF can also reduce levels of IL-1β, TNF-α and IL-6. Further studies showed that triterpene saponins from CFAF induced anti-inflammatory activity inhibited inflammatory mediators by blocking JAK/STAT signalling pathways in the LPS-treated macrophages. [ABSTRACT FROM AUTHOR]

A new demethyl abietane diterpenoid, Triptotin K (3) together with three known compounds, friedelin (1), canophyllal (2), and triptonoterpene (4) were isolated from the roots of Tripterygium wilfordii Hook. f. by silica gel column and preparative high performance liquid chromatography. Their structures were determined by extensive NMR data and mass spectroscopic analysis. Triptotin K showed cytotoxic activities against KB, KBv200, HepG2, and MCF-7/ADM cells lines with IC50 values of 29.88, 36.50, 39.55, and 41.38 μM, respectively. [ABSTRACT FROM AUTHOR]

One new indole-type alkaloid, α-L-rhamnopyranosyl-(1→6)-β-D- glucopyranosyl 6-methoxy-3-indolecarbonate (1), together with three known alkaloids (2–4), one aromatic acid (5) and five known saponins (6–10), was isolated from the roots of Clematis florida var. plena. Their structures were established by NMR spectroscopic analysis and acid hydrolysis. In in vivo anti-inflammatory activity, n-butanol extract was found to be potent against ear edema in mice, with inhibition rate of 48.7% at a dose of 800 mg/kg. Furthermore, compounds 8 and 9 obtained from the n-butanol extract exhibited significant anti-inflammatory activities with inhibition rates of 50.9% and 54.7% at a dose of 200 mg/kg. [ABSTRACT FROM AUTHOR]

Two new phenylspirodrimanes, stachybotrin H (1) and stachybotrysin H (9) together with eleven known analogues (2–8, 10–13) were isolated from deep-sea derived Stachybotrys sp. MCCC 3A00409. Their structures were determined by extensive NMR data and mass spectroscopic analysis. Compounds 9–12 showed weak cytotoxicity against three human cancer cell lines K562, Hela and HL60 with IC50 in the range of 18.5–52.8 μM. [ABSTRACT FROM AUTHOR]

Background Although the nicotinamide adenine dinucleotide (NAD + )/CD38/cyclic ADP ribose (cADPR)/Ca 2+ signaling pathway has been shown to regulate intracellular calcium homeostasis and functions in multiple inflammatory processes, its role in sepsis remains unknown. The aim of this study was to determine whether the NAD + /CD38/cADPR/Ca 2+ signaling pathway is activated during sepsis and whether an inhibitor of this pathway, 8-Br-cADPR, protects the organs from sepsis-induced damage. Materials and methods Male Sprague–Dawley rats were subjected to cecal ligation and puncture (CLP) or sham laparotomies. NAD + , cADPR, CD38, and intracellular Ca 2+ levels were measured in the hearts, livers, and kidneys of septic rats at 0, 6, 12, 24, and 48 h after CLP surgery. Rats were also divided into sham, CLP, and CLP+8-Br-cADPR groups, and the hearts, livers, and kidneys were hematoxylin–eosin-stained and assayed for malondialdehyde and superoxide dismutase activities. Results NAD + , cADPR, CD38, and intracellular Ca 2+ levels increased in the hearts, livers, and kidneys of septic rats as early as 6–24 h after CLP surgery. Treatment with 8-Br-cADPR inhibited sepsis-induced intracellular Ca 2+ mobilization, attenuated tissue injury, reduced malondialdehyde levels, and increased superoxide dismutase activity in septic rats. Conclusions The NAD + /CD38/cADPR/Ca 2+ signaling pathway was activated during sepsis in the CLP rat model. Blocking this pathway with 8-Br-cADPR protected hearts, livers, and kidneys from sepsis-induced damage. [ABSTRACT FROM AUTHOR]

The phytochemical study of the fruits of Melia azedarach (Meliaceae) led to the isolation and characterisation of two novel natural limonoids1-deoxy- 3, 20-dicinnamoyl-11-methoxy-meliacarpinin ( 1 ) and 12 β - O- methyl nimbolinin A ( 2 ), along with twelve known limonoids. Its structure was identified by 1D- and 2D-NMR, HR-ESI-MS and comparison with published data. The anti-inflammatory effect of the compounds was measured in vitro in RAW 264.7 cells by evaluating the production of NO stimulated by LPS. Compounds 1, 8 and 14 indicated significant anti-inflammatory effect with inhibition rate of 11.76, 8.45 and 6.59 μM, respectively. Limonoid 1 significantly inhibited the production of NO, TNF- α and IL-1 β in RAW 264.7 cells. Therefore, limonoid derivative may be a promising source of bioactive metabolite for inflammatory diseases.

Mast cells (MCs) have emerged as pivotal contributors to both the defensive immune response and immunomodulation. They also exhibit regulatory functions in modulating pathological processes across various allergic diseases. The impact of MC presence within tumor tissues has garnered considerable attention, yielding conflicting findings. While some studies propose that MCs within tumor tissues promote tumor initiation and progression, others advocate an opposing perspective. Notably, evidence emphasizes the dual role of MCs in cancer, both as promoters and suppressors, is crucial for optimizing cancer treatment strategies. These conflicting viewpoints have generated substantial controversy, underscoring the need for a comprehensive understanding of MC's role in tumor immune responses., Competing Interests: None., (AJCR Copyright © 2024.)

Based on its absence in normal tissues and its role in tumorigenesis and tumor progression, insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), a reader of N6-methyladenosine (M 6 A) on RNA, represents a putative valuable and specific target for some cancer therapy. In this study, we performed bioinformatic analysis and immunohistochemistry (IHC) to find that IGF2BP3 was highly expressed in tumor epithelial cells and fibroblasts of ovarian cancer (OC), and was associated with poor prognosis, metastasis, and chemosensitivity in OC patients. In particular, we discovered that knockdown IGF2BP3 expression inhibited the malignant phenotype of OC cell lines by decreasing the protein levels of c-MYC, VEGF, CDK2, CDK6, and STAT1. To explore the feasibility of IGF2BP3 as a therapeutic target for OC, a small molecular AE-848 was designed and screened by molecular operating environment (MOE), which not only could duplicate the above results of knockdown assay but also reduced the expression of c-MYC in M2 macrophages and tumor-associated macrophages and promoted the cytokine IFN-γ and TNF-α secretion. The pharmacodynamic models of two kinds of OC bearing animals were suggested that systemic therapy with AE-848 significantly inhibited tumor growth by reducing the expression of tumor-associated antigen (c-MYC/VEGF/Ki67/CDK2) and improving the anti-tumor effect of macrophages. These results suggest that AE-848 can inhibit the growth and progression of OC cells by disrupting the stability of the targeted mRNAs of IGF2BP3 and may be a targeted drug for OC treatment., Competing Interests: None., (AJCR Copyright © 2023.)

There are very few published studies in the literature examining the association between vitiligo and skin cancers and only some anecdotal reports about phototherapy-associated nonmelanoma skin carcinoma (NMSC) in patients with vitiligo. Herein, we report a case of an 84-year-old male with widespread vitiligo with concurrent onset of two primary cutaneous malignancies in sun-exposed vitiligo skin. The association between vitiligo and NMSC deserves further assessment. Chronic sun damage might be a possible causative factor for the development of NMSC in the vitiligo patient., Competing Interests: There are no conflicts of interest. What is new? Multiple cutaneous malignancies concurrence in vitiligo-affected skin on sun-exposed areas in a Fitzpatrick Skin Type III patient with widespread vitiligo without psoralen–ultraviole (UV)-A or narrow-band UV-B therapy are rare, Cumulative UV in patients with vitiligo may still be a risk factor for nonmelanoma skin carcinoma.

The title compound [systematic name: (4b S )-4-hy-droxy-2-isopropyl-4b,8,8-trimethyl-4b,5,6,7,8,8a-hexa-hydro-phenanthrene-3,9-dione], C 20 H 26 O 3 , is an abietane-type diterpene, which was isolated from Taxodium ascendens (B.). In the crystal, mol-ecules are linked by weak C-H⋯O hydrogen bonds, forming supra-molecular chains propagating along the [001] direction.

Pre-B cell colony-enhancing factor (PBEF) has been shown to have a variety of biological functions. Studies have proven that PBEF plays a functional role in acute lung injury (ALI). Therefore, in this study, we aimed to confirm the importance of PBEF in ALI. The effects of PBEF overexpression on the apoptosis of human pulmonary microvascular endothelial cells (HPMECs) were analyzed by flow cytometry, and the results indicated that PBEF promoted the apoptosis of HPMECs, which aggravated the development of ALI. Comparative experiments involving increasing and decreasing PBEF expression demonstrated that PBEF promoted the expression of inflammatory factors, such as interleukin (IL)‑1β, IL‑6 and IL‑8 in the HPMECs , thus intensifying the inflammatory response. PBEF also inhibited the expression of aquaporin 1 (AQP1), which caused a dysfunction and imbalance in water transport. Moreover, we also found that tumor necrosis factor (TNF)‑α promoted the expression of PBEF in the HPMECs. After blocking the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) pathways, we found that PBEF regulated the expression of inflammatory factors and AQP1, mainly through the MAPK pathways. Taken together, these results demonstrate that the increase in intracellular PBEF expression promoted the apoptosis of HPMECs and the expression of inflammatory factors and thus enhanced the inflammatory response and inhibited the expression of AQP1, which resulted in abnormal water transport, diminishing the regulatory effects of AQP1 on water transport.