Anti-inflammatory effects of the selective phosphodiesterase 3 inhibitor, cilostazol, and antioxidants, enzymatically-modified isoquercitrin and α-lipoic acid, reduce dextran sulphate sodium-induced colorectal mucosal injury in mice

Kangawa, Yumi; Yoshida, Toshinori; Abe, Hajime; Seto, Yoshiki; Miyashita, Taishi; Nakamura, Michi; Kihara, Tohru; Hayashi, Shim-mo; Shibutani, Makoto

doi:10.1016/j.etp.2016.12.004

Cited by 29 publications

(42 citation statements)

References 39 publications

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“…ALA or AL-1 were used as therapeutic options to cure the induced UC throughout all the studies. 47 showed that ALA (different doses) significantly reduced the TNF-α content in tissue or the plasma during the treatment course and afterward when compared with the control group. 47 showed that ALA (different doses) significantly reduced the TNF-α content in tissue or the plasma during the treatment course and afterward when compared with the control group.…”

Section: Resultsmentioning

confidence: 92%

“…50 Administration of AL-1 attenuated the body weight decline in colitis mice. 47 In Trivedi and Jena 49 study, coadministration and posttreatment of ALA significantly increased the colon length of DSS-induced UC in mice. 47 In Trivedi and Jena 49 study, coadministration and posttreatment of ALA significantly increased the colon length of DSS-induced UC in mice.…”

Section: Effect Of Ala In Comparison Withmentioning

confidence: 92%

“…47 In contrast, Sun et al 46 surveyed that the ALA treatment increased the body weight of induced UC mice. However, two investigations were conducted on rats.…”

Section: Effect Of Ala In Comparison Withmentioning

confidence: 97%

“…[47][48][49] Trivedi and Jena 49 reported that the IL-6 level was significantly declined in tissue and the plasma following the administration of specific dosages of ALA, either in cotreatment (receiving ALA before the induction of UC) or posttreatment (receiving ALA following the induction of UC) groups compared with the control mice. [47][48][49] Trivedi and Jena 49 reported that the IL-6 level was significantly declined in tissue and the plasma following the administration of specific dosages of ALA, either in cotreatment (receiving ALA before the induction of UC) or posttreatment (receiving ALA following the induction of UC) groups compared with the control mice.…”

Section: Effect Of Ala and Al-1 Inmentioning

confidence: 99%

“…[47][48][49] Trivedi and Jena 49 reported that the IL-6 level was significantly declined in tissue and the plasma following the administration of specific dosages of ALA, either in cotreatment (receiving ALA before the induction of UC) or posttreatment (receiving ALA following the induction of UC) groups compared with the control mice. 47,48 Only in one study, the IL-6 amount was determined in rat UC model. 47,48 Only in one study, the IL-6 amount was determined in rat UC model.…”

Section: Effect Of Ala and Al-1 Inmentioning

confidence: 99%

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Effects of alpha lipoic acid and its derivative “andrographolid‐lipoic acid‐1” on ulcerative colitis: A systematic review with meta‐analysis of animal studies

Moeinian

Abdolghaffari

Nikfar

et al. 2018

J of Cellular Biochemistry

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We aimed to review and meta‐analyze the inflammatory and oxidative factors following alpha lipoic acid (ALA) and its derivative “andrographolid‐lipoic acid‐1” (AL‐1) in ulcerative colitis (UC). ALA plays an important role in scavenging intracellular radicals and inflammatory elements. AL‐1 is found in herbal medicines with potent anti‐inflammatory properties. Data were collected from the Google Scholar, PubMed, Scopus, Evidence‐based medicine/clinical trials, and Cochrane library database until 2017, which finally resulted in 22 animal studies (70 rats and 162 mice). The beneficial effects of ALA or AL‐1 on the most important parameters of UC were reviewed; also, studies were considered separately in mice and rats. Administration of ALA and AL‐1 significantly reduced the tumor necrosis factor‐α level compared with the controls, while data were not noteworthy in the meta‐analysis (mean differences = −18.57 [95% CI = −42.65 to 5.51], P = 0.13). In spite of insignificant decrease in meta‐analysis outcomes (differences = 6.92 [95% CI = −39.33 to 53.16], P = 0.77), a significant reduction in myeloperoxidase activity was shown following ALA or AL‐1 treatment compared with the controls. Despite significant differences in each study, we had to exclude some studies to homogenize data for meta‐analyzing as they showed insignificant results. Interleukin 6, cyclooxygenase‐2, glutathione, malondialdehyde, superoxide dismutase, histopathological score, macroscopic and microscopic scores, disease activity index, body weight change, and colon length were also reviewed. Most studies have emphasized on significant positive effects of ALA and AL‐1. Comprehensive clinical trials are obligatory to determine the precious position of ALA or AL‐1 in the management of UC.

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Section: Resultsmentioning

confidence: 92%

Section: Effect Of Ala In Comparison Withmentioning

confidence: 92%

“…47 In contrast, Sun et al 46 surveyed that the ALA treatment increased the body weight of induced UC mice. However, two investigations were conducted on rats.…”

Section: Effect Of Ala In Comparison Withmentioning

confidence: 97%

Section: Effect Of Ala and Al-1 Inmentioning

confidence: 99%

“…[47][48][49] Trivedi and Jena 49 reported that the IL-6 level was significantly declined in tissue and the plasma following the administration of specific dosages of ALA, either in cotreatment (receiving ALA before the induction of UC) or posttreatment (receiving ALA following the induction of UC) groups compared with the control mice. 47,48 Only in one study, the IL-6 amount was determined in rat UC model. 47,48 Only in one study, the IL-6 amount was determined in rat UC model.…”

Section: Effect Of Ala and Al-1 Inmentioning

confidence: 99%

See 3 more Smart Citations

Effects of alpha lipoic acid and its derivative “andrographolid‐lipoic acid‐1” on ulcerative colitis: A systematic review with meta‐analysis of animal studies

Moeinian

Abdolghaffari

Nikfar

et al. 2018

J of Cellular Biochemistry

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Gastrointestinal Bleeding During Direct Oral Anticoagulant Therapy in Patients With Nonvalvular Atrial Fibrillation and Risk of Polypharmacy

Honda

Abe

Oda

et al. 2022

The Journal of Clinical Pharma

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Although concomitant medications have been raised as a factor affecting hemorrhage during direct oral anticoagulant (DOAC) therapy, details remain unelucidated. This study was conducted to clarify the relationship between concomitant medications with possible pharmacokinetic interactions and number of concomitant medications, and bleeding and embolism in patients with nonvalvular atrial fibrillation on DOACs. The subjects were 1010 patients prescribed DOACs from a single‐center at the Teikyo University Hospital between April 2011 and June 2018. This study was an exploratory analysis and investigated their course between the first prescription and December 2018, including the presence or absence of clinically relevant bleeding, gastrointestinal bleeding, and major cardiovascular and cerebrovascular events. Impacts of medications were evaluated by the general linear model with inverse probability‐weighted propensity score. The observation period was 2272 patient‐years. The rate of bleeding was 4.7%/year, gastrointestinal bleeding was 2.8%/year, and major cardiovascular and cerebrovascular events were 2.0%/year. Taking 10 or more oral medications concurrently was a significant risk for gastrointestinal bleeding (hazard ratio, 2.046 [95%CI, 1.188‐3.526]; P = .010). Nonsteroidal anti‐inflammatory drugs were the only significant risk for gastrointestinal bleeding. Clinicians should be aware of gastrointestinal bleeding when using DOACs with patients taking more than 10 medications and/or nonsteroidal anti‐inflammatory drugs.

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Cilostazol against 2,4,6‐trinitrobenzene sulfonic acid‐induced colitis: Effect on tight junction, inflammation, and apoptosis

Al‐Kishali

Fattah

Mohammad³

et al. 2019

JGH Open

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Background Inflammatory bowel diseases are immunologically mediated disorders of gastrointestinal tract, characterized by dysregulated immune responses that result in a chronic intestinal inflammation. The antiplatelet cilostazol (CS), a phosphodiesterase‐III inhibitor, exerted a beneficial effect on several models of gastrointestinal diseases; however, the full mechanism of action in this context has not been unveiled. Aim The current study aimed to elucidate the potential role of CS in a 2,4,6‐trinitrobenzene sulfonic acid (TNBS)‐induced colitis model. Methods Male Wistar rats were divided into a sham group and groups treated with sulfasalazine (500 mg/kg), CS (50 and 100 mg/kg), and a combination (sulfasalazine/CS 50 mg/kg). All treatments were administered orally 15 days, with TNBS rectal administration on the 11th day. Results TNBS‐produced colitis manifested as a decrease in the epithelial junctional adhesion molecule‐A (JAM‐A) and as an increase in trefoil factor‐3, ulcerative area, and colon mass index, parameters that collaborate with the gross macroscopic changes in colon tissue. In addition, TNBS increased hemeoxygenase‐1, nuclear factor‐kappa B, P‐selectin, and myeloperoxidase, as well as the apoptotic ratio of Bax/Bcl‐2. Administration of CS alone, especially at the high dose level, attenuated the severity of TNBS‐induced colitis in a sulfasalazine‐comparable manner. In addition, a better effect was mediated by the combination regimen, which succeeded in normalizing most of the measured parameters. Conclusion CS protected the colon against TNBS through its anti‐inflammatory and antiapoptotic effects along with maintaining cellular tight junctions (TJs). Furthermore, CS can be beneficial as an add‐on drug with the conventional treatments of colitis.

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Anti-inflammatory effects of the selective phosphodiesterase 3 inhibitor, cilostazol, and antioxidants, enzymatically-modified isoquercitrin and α-lipoic acid, reduce dextran sulphate sodium-induced colorectal mucosal injury in mice

Cited by 29 publications

References 39 publications

Effects of alpha lipoic acid and its derivative “andrographolid‐lipoic acid‐1” on ulcerative colitis: A systematic review with meta‐analysis of animal studies

Effects of alpha lipoic acid and its derivative “andrographolid‐lipoic acid‐1” on ulcerative colitis: A systematic review with meta‐analysis of animal studies

Gastrointestinal Bleeding During Direct Oral Anticoagulant Therapy in Patients With Nonvalvular Atrial Fibrillation and Risk of Polypharmacy

Cilostazol against 2,4,6‐trinitrobenzene sulfonic acid‐induced colitis: Effect on tight junction, inflammation, and apoptosis

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