Immunomodulatory effects of nanocurcumin in arsenic-exposed rats

Sankar, P.; Telang, A.G.; Suresh, Subramaniyam; Kesavan, Manickam; Kandasamy, Kannan; Kalaivanan, Ramya; Sarkar, Srobana

doi:10.1016/j.intimp.2013.05.019

Cited by 34 publications

(19 citation statements)

References 56 publications

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“…These changes may cause cellular dysfunction due to the development of inflammatory reactions and the secretion of a variety of inflammatory cytokines. Several lines of study have also shown that supplementation of dietary antioxidants may reverse arsenic-induced oxidative damage andimmunotoxicity [30]. Accumulating evidence has revealed that EGCG, as a potent antioxidative agent, can inhibit inflammation and enhance the survival of disc cells in oxidative stress [31].…”

Section: Discussionmentioning

confidence: 99%

(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

Yu¹,

Pei

Huang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Exposure to arsenic in individuals has been found to be associated with various health-related problems including skin lesions, cancer, and cardiovascular and immunological disorders. (-)-Epigallocatechin-3-gallate (EGCG), the main and active polyphenolic catechin present in green tea, has shown potent antioxidant, anti-apoptotic and anti-inflammatory activity in vivo and in vitro. Thus, the present study was conducted to investigate the protective effects of EGCG against arsenic-induced inflammation and immunotoxicity in mice. Methods: Serum IL-1β, IL-6 and TNF-α were determined by ELISA, tissue catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide and caspase 3 by commercial kits, mitochondrial membrane potential with Rh 123, mitochondrial ROS with 2’,7’-dichlorofluorescin diacetate (DCFH-DA), apoptotic and necrotic cells and T-cell phenotyping with Flow cytometry analysis. Results: The results showed that arsenic treatment significantly increased oxidative stress levels (as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione and reactive oxygen species), increased levels of inflammatory cytokines and promoted apoptosis. Arsenic exposure increased the relative frequency of the CD8+(Tc) cell subpopulation (from 2.8 to 18.9%) and decreased the frequency of CD4+(Th) cells (from 5.2 to 2.7%). Arsenic exposure also significantly decreased the frequency of T(CD3) (from 32.5% to 19.2%) and B(CD19) cells (from 55.1 to 32.5%). All of these effects induced by NaAsO₂ were attenuated by EGCG. Conclusions: The present in vitro findings indicate that EGCG attenuates not only NaAsO₂-induced immunosuppression but also inflammation and apoptosis.

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Section: Discussionmentioning

confidence: 99%

(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

Yu¹,

Pei

Huang³

et al. 2017

Cell Physiol Biochem

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“…Characterization of nanoparticle-encapsulated curcumin Details regarding preparation of CUR-NP, encapsulation efficiency and particle size have been given in our earlier report [23,24]. For further characterization, we assessed release of curcumin from nanoparticles and its solubility.…”

Section: Methodsmentioning

confidence: 99%

“…Details regarding the chemicals and reagents, animal management and basis of selection of curcumin dose and arsenic concentration have been reported earlier [23,24]. Rats were randomly divided into 5 groups of 12 each.…”

Section: Chemicals Animals and Experimental Designmentioning

confidence: 99%

Protective action of curcumin and nano-curcumin against arsenic-induced genotoxicity in rats in vivo

et al. 2014

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We explored whether nanoformulation of curcumin can cause better protective effect than free curcumin against arsenic-induced genotoxicity. Curcumin-loaded Poly(lactic-co-glycolic acid) nanoparticles (CUR-NP) were prepared by emulsion technique. The CUR-NP were water soluble and showed biphasic release pattern. Rats were divided into 5 groups of 6 each. Group I served as the control. Group II rats were exposed to sodium arsenite (25 ppm) daily through drinking water for 42 days. Groups III, IV and V were maintained as in Group II, however, they were also administered empty nanoparticle, curcumin (100 mg/kg bw) and CUR-NP (100 mg/kg bw), respectively, by oral gavage during the last 14 days of arsenic exposure. On the 43rd day, genotoxic effects were evaluated in bone marrow cells. Arsenic increased chromosomal aberrations, micronuclei formation and DNA damage. Both free curcumin and CUR-NP attenuated these arsenic-mediated genotoxic effects. However, the result suggests that nanoformulation have better protective effect than free curcumin at the same dose level.

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“…16 The inflammatory effect of TGF-β promotes in the presence of IL-6, which causes the development of Th17 lymphocytes from naïve T cells and induces further inflammation in the body. 10,21,22 Consequently, the aim of the current study was to examine the possible mechanisms of nanocurcumin action in AS therapy. 19 Previous studies have reported upregulation of TGF-β and IL-6 in AS patients.…”

Section: Introductionmentioning

confidence: 99%

The effects of nanocurcumin on Treg cell responses and treatment of ankylosing spondylitis patients: A randomized, double‐blind, placebo‐controlled clinical trial

Ahmadi

Hajialilo

Eghbal‐Fard

et al. 2019

J of Cellular Biochemistry

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Aim Ankylosing spondylitis (AS) is an inflammatory rheumatic disease with increased bone mass in the main sites of inflammation. Regulatory T (Treg) cells have been reported to involve in pathology of AS. This study designed at investigating the effects of nanocurcumin on Treg cell responses in peripheral blood (PB) of AS patients. Methods Test group including 12 AS patients received nanocurcumin daily for 4 months and control group including 12 patients received placebo. The frequency of Treg was measured by flow cytometry. The expression levels of FoxP3 and several associated microRNAs (miRNAs; miR‐27, miR‐17, and miR‐146a) and cytokines including Interleukin‐10 (IL‐10), TGF‐β, and IL‐6 were assessed by real‐time polymerase chain reaction. Furthermore, enzyme‐linked immunosorbent assay was done to determine the secretion levels of cytokines. Results After treatment with nanocurcumin the frequency of Treg cells in AS patients increased significantly. The RT‐PCR data indicated that the expression of miR‐17 and miR‐27 were significantly decreased following nanocurcumin treatment while miR‐146a and FoxP3 were significantly increased. Moreover, nanocurcumin‐treated group had high levels of IL‐10 and TGF‐β and low levels of IL‐6 production than control group. Conclusion The findings suggested that dysregulation of Treg cells in PB influences the AS development and nanocurcumin therapy could regulate the Treg cells, and so could be useful in the treatment of AS and may be other autoimmune diseases. This study is registered with IRCT.ir, number IRCT2017052927520N7.

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Immunomodulatory effects of nanocurcumin in arsenic-exposed rats

Cited by 34 publications

References 56 publications

(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

Protective action of curcumin and nano-curcumin against arsenic-induced genotoxicity in rats in vivo

The effects of nanocurcumin on Treg cell responses and treatment of ankylosing spondylitis patients: A randomized, double‐blind, placebo‐controlled clinical trial

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