ABSTRACT
The present study aimed to investigate the antiarthritic effects of curculigoside isolated from the rhizome of Curculigo orchioides Gaertn in vivo and in vitro, as well as to determine the potential underlying mechanisms. A rat model of arthritis was induced with type II collagen. Arthritic rats were treated with curculigoside (50 mg/kg) and blood samples were collected to determine serum levels of tumor necrosis factor (TNF)α, interleukin (IL)1ß, IL6, IL10, IL12 and IL17A. Furthermore, indices of the thymus and spleen were determined. The antiproliferative effects of curculigoside were detected with Cell Counting kit8 assays in rheumatoid arthritisderived fibroblastlike synoviocyte MH7A cells. In addition, expression levels of Janus kinase (JAK)1, JAK3, signal transducer and activator of transcription (STAT)3, nuclear factor (NF)κB p65 and its inhibitor (IκB) were determined by western blotting. The results revealed that curculigoside inhibited paw swelling and arthritis scores in type II collageninduced arthritic (CIA) rats. Additionally, curculigoside decreased serum levels of TNFα, IL1ß, IL6, IL10, IL12 and IL17A in CIA rats. Curculigoside also significantly inhibited MH7A cell proliferation in a time and concentrationdependent manner. Furthermore, treatment downregulated the expression of JAK1, JAK3 and STAT3, and upregulated cytosolic nuclear factor (NF)κB p65 and IκB. In conclusion, the results of the present study indicated that curculigoside exhibited significant antiarthritic effects in vivo and in vitro, and the molecular mechanism may be associated with the JAK/STAT/NFκB signaling pathway.
Subject(s)
Arthritis, Rheumatoid/drug therapy , Benzoates/administration & dosage , Glucosides/administration & dosage , Janus Kinase 1/genetics , Janus Kinase 3/genetics , STAT3 Transcription Factor/genetics , Animals , Arthritis, Rheumatoid/chemically induced , Arthritis, Rheumatoid/genetics , Arthritis, Rheumatoid/pathology , Cell Proliferation/drug effects , Collagen Type II/toxicity , Disease Models, Animal , Gene Expression/drug effects , Humans , I-kappa B Proteins/genetics , Interleukins/genetics , Rats , Signal Transduction , Synoviocytes/drug effects , Transcription Factor RelA/genetics , Tumor Necrosis Factor-alpha/geneticsABSTRACT
Attribute-based encryption (ABE) is a popular cryptographic technology to protect the security of users' data in cloud computing. In order to reduce its decryption cost, outsourcing the decryption of ciphertexts is an available method, which enables users to outsource a large number of decryption operations to the cloud service provider. To guarantee the correctness of transformed ciphertexts computed by the cloud server via the outsourced decryption, it is necessary to check the correctness of the outsourced decryption to ensure security for the data of users. Recently, Li et al. proposed a full verifiability of the outsourced decryption of ABE scheme (ABE-VOD) for the authorized users and unauthorized users, which can simultaneously check the correctness of the transformed ciphertext for both them. However, in this paper we show that their ABE-VOD scheme cannot obtain the results which they had shown, such as finding out all invalid ciphertexts, and checking the correctness of the transformed ciphertext for the authorized user via checking it for the unauthorized user. We first construct some invalid ciphertexts which can pass the validity checking in the decryption algorithm. That means their "verify-then-decrypt" skill is unavailable. Next, we show that the method to check the validity of the outsourced decryption for the authorized users via checking it for the unauthorized users is not always correct. That is to say, there exist some invalid ciphertexts which can pass the validity checking for the unauthorized user, but cannot pass the validity checking for the authorized user.
