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Castleman disease (CD) is clinically divided into unicentric CD (UCD) and multicentric CD (MCD). Hyaline-vascular variant (HV) is the most common pathological type of UCD, while the plasma cell type (PC) is the most common type of MCD and thus, hyaline-vascular variant multicentric CD (HV-MCD) is a rare type of CD. In addition, its etiology has remained elusive. The present study retrospectively analyzed the medical records of 3 patients diagnosed as HV-MCD admitted to The First Affiliated Hospital of Guangxi Medical University (Guangxi, China) between January 2007 and September 2020. A total of 2 males and 1 female were admitted. The areas involved varied considerably. Respiratory symptoms were seen in 3 cases, along with fever, weight loss and splenomegaly. Damage to the skin and mucous membranes resulted in oral ulcers when accompanied by paraneoplastic pemphigus (PNP). Dry and wet rales were found in all patients. All 3 cases were complicated with PNP and had hypoxemia and obstructive ventilation dysfunction. In accordance with PC-MCD, it manifested as lymph node enlargement and may involve several lymph nodes. Computed tomography mainly indicated bronchiectasis and mediastinal lymph node enlargement. In 1 case, chemotherapy failed after local mass excision, 1 case remitted after chemotherapy but the lung lesion was irreversible and 1 case was untreated and soon died of respiratory failure. The cases of HV-MCD with pulmonary involvement were induced by small airway lesions and associated with poor prognosis. Respiratory symptoms along with systemic symptoms were common. [ABSTRACT FROM AUTHOR]

Evodiamine (Evo) is an alkaloid that can be extracted from the berry fruit Evodia rutaecarpa and has been reported to exert various pharmacological effects, such as antidiarrheal, antiemetic and antiulcer effects. In vivo, the potential effects of Evo were investigated in a mouse model of dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) and in adenomatous polyposis coli (Apc)MinC/Gpt C57BL/6 mice with colorectal cancer (CRC), where the latter harbours a point-mutation in the Apc gene. Evo suppressed the degree of weight loss and colon shortening induced by DSS, decreased the disease activity index value and ameliorated the pathological alterations in the colon of mice with UC as examined via H&E staining of colon tissues. In addition, Evo decreased the number and size of colonic tumors in ApcMinC/Gpt mice. Proteomics (colon tissues), ELISA (colon tissues and serum) and western blotting (colon tissues) results revealed that Evo inhibited NF-κB to mediate the levels of various cytokines, including, in the DSS-induced UC model, IL-1β, IL-2, IL-6, IL-8, TNF-α, IFN-γ (ELISA of colon tissues and serum), NF-κB, IKKα+β, IκBα, S100a9, TLR4 and MyD88 (western blotting of colon tissues), and, in the colorectal cancer model, IL-1β, IL-2, IL-6, IL-15, IL-17, IL-22, TNF-α (ELISA of colon tissues and serum), NF-κB, IKKα+β, IκBα and S100a9 (western blotting of colon tissues), to achieve its anti-inflammatory and antitumor effects. In vitro, Evo also reduced the viability of the colon cancer cell line SW480, inhibited mitochondrial membrane potential (MMP detection), caused G2/M-phase arrest (cell cycle detection) and suppressed the translocation of phosphorylated-NF-κB from the cytoplasm into the nucleus (immunofluorescence of p-NF-κB). Theoretical evidence (MD simulations) suggest that Evo may bind to the ordered domain (α-helix) of NF-κB to influence this protein. The protein secondary structure changes were analyzed by the cpptraj module in Amber. In addition, these data provide experimental evidence that Evo may be an effective agent for treating UC and CRC. [ABSTRACT FROM AUTHOR]