Salicin from <i>Alangium chinense</i> Ameliorates Rheumatoid Arthritis by Modulating the Nrf2-HO-1-ROS Pathways

Zhai, Kefeng; Duan, Hong; Khan, Ghulam Jilany; Xu, Hui; Han, Fang-Kai; Cao, Wen-gen; Gao, Guizhen; Shan, Lingling; Wei, Zhao‐Jun

doi:10.1021/acs.jafc.8b02241

Cited by 101 publications

(69 citation statements)

References 41 publications

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“…As an end product of peroxidization of polyunsaturated fatty acids in the membrane, MDA is attacked by oxygen free radicals; therefore, the content of MDA can reflect the degree of lipid peroxidization. As free radical-scavenging enzymes, SOD, GSH-Px and CAT act as the first line of defense against oxidative stress by eliminating reactive oxygen radicals (45). In the present study, treatment with G-Rb3/Rb2 (20 mg/kg), G-Rb3 (20 mg/kg) and DLZ (20 mg/kg) reduced the MIRI-induced elevation in MDA content, and increased the activities of SOD, GSH-Px and CAT.…”

Section: Discussionmentioning

confidence: 99%

Combination of the ginsenosides Rb3 and Rb2 exerts protective effects against myocardial ischemia reperfusion injury in rats

Liu

Jiang

et al. 2019

Int J Mol Med

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Ginsenoside Rb3 (G-Rb3) has been demonstrated to alleviate myocardial ischemia reperfusion injury (MIRI); however, it is difficult to separate G-Rb2 from its isomer G-Rb3. The current study aimed to compare the cardioprotective effects of G-Rb3 and the concomitant use of G-Rb3 and G-Rb2 (G-Rb3/Rb2) on MIRI in rats. A rat model of MIRI was established by ligation of the left anterior descending coronary artery and the rats were randomly divided into five groups. Prior to MIRI, G-Rb3/Rb2 (20 mg/kg), G-Rb3 (20 mg/kg) and diltiazem (DLZ; 20 mg/kg, as a positive control) were orally administered to the rats once a day for 3 consecutive days. After 30 min of ischemia and 120 min of reperfusion, cardiac function, infarct size, cardiac marker enzymes, antioxidative parameters, inflammatory factors, histopathological changes, cardiomyocyte apoptosis, and B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein and caspase-3 expression were determined using a multi-channel physiological recording system, nitrotetrazolium blue chloride, biochemical kits, radioimmunoassay kits, hematoxylin and eosin, terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay, immunohistochemistry and reverse transcription-quantitative PCR, respectively. The results indicated that treatment with G-Rb3/Rb2 significantly protected rats against MIRI, as shown by improved cardiac function, reduced myocardial ischemic area, decreased serum activities of aspartate aminotransferase, lactate dehydrogenase and creatine kinase MB, decreased serum concentrations of interleukin-6 and tumor necrosis factor-α, decreased malondialdehyde concentration in myocardial tissues, increased activities of superoxide dismutase, glutathione peroxidase and catalase in myocardial tissues, reduced histopathological changes in myocardial tissues, reduced number of apoptotic cardiomyocytes, and changes in the expression levels of caspase-3, Bcl-2 and Bax. In addition, the effects of treatment with G-Rb3/Rb2, G-Rb3 or DLZ were equivalent. The protective effects of G-Rb3/Rb2 on MIRI were similar to those of G-Rb3 in terms of oxidative stress, inflammatory factors and inhibition of cardiomyocyte apoptosis. Therefore, G-Rb3/Rb2 may be developed as a concomitant treatment for MIRI.

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Section: Discussionmentioning

confidence: 99%

Combination of the ginsenosides Rb3 and Rb2 exerts protective effects against myocardial ischemia reperfusion injury in rats

Liu

Jiang

et al. 2019

Int J Mol Med

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“…D21490; Invitrogen; Thermo Fisher Scientific, Inc.) at room temperature in the dark for 5 min. Cells were imaged using a fluorescence photomicroscope (IX51; Olympus Corporation; magnification ×400) and analyzed with Image-Pro Plus 6.0 software (Media Cybernetics, Inc.) (24).…”

Section: Methodsmentioning

confidence: 99%

“…Western blotting was conducted as previously described (24). Proteins (30 µg) were separated via 10% SDS-PAGE under reducing conditions, and transferred onto nitrocellulose membranes.…”

Section: Methodsmentioning

confidence: 99%

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Urate transport capacity of glucose transporter 9 and urate transporter 1 in cartilage chondrocytes

et al. 2019

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Chronic gouty arthritis, caused by a persistent increase in, and the deposition of, soluble uric acid (sUA), can induce pathological chondrocyte destruction; however, the effects of urate transport and intracellular sUA on chondrocyte functionality and viability are yet to be fully determined. Thus, the aim of the present study was to investigate the presence and functionality of a urate transport system in chondrocytes. The expression profiles of two primary urate reabsorptive transporters, glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1), in human articular cartilage and chondrocyte cell lines were examined via western blotting, reverse transcription-quantitative PCR, immunohistochemistry and immunofluorescence. Then, chondrocytes were incubated with exogenous sUA at increasing concentrations. Negative control assays were conducted via the specific knockdown of GLUT9 and URAT1 with lentiviral short hairpin (sh)RNAs, and by pretreatment with benzbromarone, a known inhibitor of the two transporters. Intracellular UA concentrations were measured using colorimetric assays. The expression levels of GLUT9 and URAT1 were determined in cartilage tissues and chondrocyte cell lines. Incubation of chondrocytes with sUA led to a concentration-dependent increase in intracellular urate concentrations, which was inhibited by GLUT9 or URAT1 knockdown, or by benzbromarone pretreatment (27.13±2.70, 44.22±2.34 and 58.46±2.32% reduction, respectively). In particular, benzbromarone further decreased the already-reduced intracellular UA concentrations in HC-shGLUT9 and HC-shURAT1 cells by 46.79±2.46 and 39.79±2.22%, respectively. Cells overexpressing GLUT9 and URAT1 were used as the positive cell control, which showed increased intracellular UA concentrations that could be reversed by treatment with benzbromarone. In conclusion, chondrocytes may possess an active UA transport system. GLUT9 and URAT1 functioned synergistically to transport UA into the chondrocyte cytoplasm, which was inhibited by specific gene knockdowns and drug-induced inhibition. These results may be fundamental in the further investigation of the pathological changes to chondrocytes induced by sUA during gouty arthritis, and identified UA transport processes as potential targets for the early control of chronic gouty arthritis.

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“…Ample evidence supports the notion that HO-1 can confer protection against oxidative stress and in ammatory and immune responses in joint tissues, which pathway may control the activation and metabolism of articular cells [23]. A previous study showed that salicin ameliorates rheumatoid arthritis by promoting HO-1 expression in RA-FLSs [24]. In our study, a low expression of HO-1 was observed in RA-FLSs and pretreatment of Gal could elevate HO-1 expression in the presence or absence of TNF-α.…”

Section: Discussionmentioning

confidence: 87%

Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway

GUAN

ZHAO

LIU

et al. 2020

Preprint

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Objective: Galuteolin (Galu) is a substance extracted and purified from honeysuckle. The purpose of this study was to explore the effects of Galu on the TNF-α-induced RA-FLS cells (synoviocytes) and reveal its potential molecular mechanism from the perspectives of anti-apoptosis and anti-inflammation.Methods: After TNF-α stimulation, cell proliferation of RA-FLS was assessed by CCK-8 assay. TUNEL staining was used to detect the apoptosis. Western Blot was used to detect the expressions of Iκκβ, p-p65, p65, p-IκB, IκB, Cleaved-caspase3, Caspase-3, Bcl-2, and Bax. HO-1 were determined by RT-PCR. The contents of pro-inflammatory cytokines IL-1β, IL-6, IL-8 and MMP-1 were determined by ELISA.Results: Galu significantly suppressed cell proliferation in a dose-dependent manner. Additionally, Galu obviously promote cell apoptosis rate of RA-FLS cells and elevated the expression levels of HO-1, caspase-3 and Bax, while reduced the expression level of Bcl-2. Furthermore, Galu apparently inhibited the levels of Iκκβ, p-p65 and p-IκB. Moreover, Galu also significantly reduced the levels of pro-inflammatory factors IL-1β, IL-6, IL-8 and MMP-1 in RA-FLS cells. Conclusion: Galuteolin exerts protective effects against TNF-α-induced RA-FLS cells by inhibiting apoptosis and inflammation, which can guide the clinical use of rheumatoid arthritis.

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Salicin from Alangium chinense Ameliorates Rheumatoid Arthritis by Modulating the Nrf2-HO-1-ROS Pathways

Cited by 101 publications

References 41 publications

Combination of the ginsenosides Rb3 and Rb2 exerts protective effects against myocardial ischemia reperfusion injury in rats

Combination of the ginsenosides Rb3 and Rb2 exerts protective effects against myocardial ischemia reperfusion injury in rats

Urate transport capacity of glucose transporter 9 and urate transporter 1 in cartilage chondrocytes

Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway

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