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A Short Review on 6-Shogaol

Review Article | DOI: https://doi.org/10.31579/2690-8816/078

A Short Review on 6-Shogaol

  • Md. Mizanur Rahaman *
  • Touhidul Islam Tanim
  • Muhammad Torequl Islam

Department of Pharmacy, life science faculty, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj-8100(Dhaka), Bangladesh.

*Corresponding Author: Md. Mizanur Rahaman, Final Department of Pharmacy, life science faculty, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj-8100(Dhaka), Bangladesh.

Citation: Md. Mizanur R, Touhidul I. Tanim and Muhammad T. Islam, (2023), A Short Review on 6-Shogaol, J. Clinical Research Notes, 4(1); DOI: 10.31579/2690-8816/078

Copyright: © 2023 Md. Mizanur Rahaman, this is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Received: 23 November 2022 | Accepted: 22 December 2022 | Published: 03 January 2023

Keywords: 6-shogaol; zingiber officinale roscoe; ginger; cancer

Abstract

The major bioactive component of dried ginger, 6-shogaol, has been utilized extensively to treat a variety of conditions. It also contributes significantly to the pungent flavor, and its precursor before dehydration is 6-gingerol, which is thought to be responsible for the biological activity and pungent flavor of fresh ginger. Gingerols, including 6-gingerol, are β-hydroxyl ketone molecules that are susceptible to dehydrating to produce an, α, β-unsaturated ketone in heat and/or acidic environments. The conjugation of the, α, β-unsaturated ketone skeleton in 6-shogaol's chemical structure explains that it's much more potent and effective than 6-gingerol in regards of antioxidant, anti-inflammatory, anticancer, antiemetic, and other bioactivities.

Introduction

6-Shogaol is principally a pungent agent that is isolated from ginger Roscoe (Han et al., 2017). The family and genus of ginger (Zingiber officinale Roscoe) is Zingiberaceaeaceae & Zingiber (Han et al., 2012). The bioactive chemical parts of ginger are primarily synthetic resin & hydrocarbon compounds. Various bioactivities that are found from ginger are gingerols, shogaols and paradols that are mainly synthetic resin compounds (Stoner et al., 2015). The chemical formulation of 6-Shogaol is C17H24O3. 6-Shogaol are often used for reducing nausea & innate reflex at early physiological state per some clinical trials. It occupies a large variety of biological activities as well as anti-cancer, corpulence-preventive & GI protective (Zhang et al., 2020). It has also anticatabolic & anti-inflammatory drug properties. It has the potential to regulate the immune responses & additionally employed in the treatment of osteoarthritis (Villavilla et al., 2013). In conclusion this review indicate to find out the protective and therapeutic potential of 6-Shogoal.

6-Shogaol

Discussion

Protective & Therapeutic Potential

Anti-oxidant property

6-Shogaol increases level of antioxidant within the liver once oral ingestion. It additionally decreases aerobic damages within the excretory organ & liver of rats (Kota et al., 2008). 6-Shogaol additionally reduces diabetic kidney disease in mice through inhibitor property (Xua et al., 2018).

Anti-inflammatory property

Anti-inflammatory drug impact is rendered by 6-Shogaol by limiting the β-hexosaminidase and inflammatory mediators while not inflicting cytotoxicity (Chen et al., 2009). 6-Shogaol additionally shows anti-inflammatory impact neuroglia that is activated by lipopolysaccharides (LPS). 6-Shogaol restricted LPS in a method that relies on concentration. It inhibits phosphorylation & nuclear translocation by limiting LPS induced NF-kB activation. This are additionally activates PPAR-γ (Peroxisome Proliferator Activated Receptor gamma) and restricted LPS induced inflammation (Han et al., 2017). It helps to decrease the extent of Nitric oxide syntheses, cyclooxygenase-2 by suppressing the discharge of cytokines. 6-Shogaol treatment suppressed Histone Deacetylase-1 expression & inflated the expression of Heat Shock Protein-70 (Shim et al., 2011).

Anti-cancer property

6-Shogaol restricted the expansion of neoplastic cell in a manner that is dose-dependent and the viability of cancer cells is reduced than in traditional cells. 6-Shogaol renders toxicity by 95% in SW480 and 90% in SW620 wherever concentration is 80µM. A combination of chemotherapeutics with 6-Shogaol will increase cell toxicity. SW480 & SW620 have cell viability 30-65%; but together with 6-shogaol will increase viability to 98%. 6-Shogaol additionally inhibits cell growth in tumuor (Woźniak et al., 2020). 6-Shogaol suppresses cell growth & proliferation in Oral epithelial cell carcinoma (OSSC). It regulates p53, Bax, Bcl-2, cleaved caspase-3 and induces caspase-mediated cell death. It additionally regulates E-cadherin & N-cadherin & occurs inhibition of OSSC cell (Huang et al., 2021). Treatment with 6-Shogaol shows antiproliferative activity in carcinoma cells. It additionally causes cell cycle accumulation in G2 phase or M phase. Furthermore it restricted autophagy in carcinoma cells. 6-Shogaol & cisplastin shows toxicity in carcinoma cell (Bawadood et al., 2020). 6-Shogaol (15 mg/kg) extensively restrained body part growth increase in transplant mouse. It restrained HCT-116 (Hematocrit-116) and SW-480 cellular proliferation with IC50 of 7.5 and 10 µM. Growth of HCT-116 cells turned into in remission on the G2/M phase of the cell cycle, in most cases mediate through the up-regulation of p53 and it also induces most cancers cell death by inducement of G2/M cell cycle arrest and caspase-mediated cell death. This compound may well be an energetic product in chemoprevention of colon cancer (L-W Qi et al., 2015). It is an α,β-unsaturated carbonyl compound of ginger led to great cytoplasmatic condition and necrobiosis in breast cancers cells (MDA-MB-231) and non-small carcinoma (A549) cells. Within the presence of autophagic inhibitors the cells persisted to showcase cytoplasmatic condition and cellular end distinctive it from the classic autophagic system while not a doubt (Nedungadi et al., 2018).

Anti-tumor property

6-Shogaol had no systemic activity.  At the dose of 50mg/kg in Hela & SiHa cells it showed remarkable growth retardation on growth volume. Mice treated with 6-shogaol had traditional blood serum concentrations of aminoalkanoic acid aminopherase (ALT), Aspartate aminopherase (AST), Alkaline Phosphate (ALP), Creatinine (CR), and Blood Urea Nitrogen (BUN). Histomorphological analysis showed that the liver, spleen and excretory organ of mice displayed no lesion or harm ensuing from drug toxicity. These results prompt that 6-shogaol restrained the Hela xenograft-tumor growth and had no harmful effects (Pei et al., 2021). The anti-tumor mechanism of 6-shogaol became determined via the induction of cellular cycle arrest and caspase-mediated cell death in human malignant hepatoma cells. It has additionally been pronounced to induce caspase-mediated cell death in human hepatocarcinoma cells once it involves proteolytic enzyme activation and endoplasmic reticulum (ER) pressure signal through PERK/eIF2a pathway. Meanwhile, 6-shogaol was founded to reduce constitutive and interlukine (IL)-6-brought about STAT3 activation at an equivalent time as inhibiting both constitutive and TNF-induced NF-kB activity to apoptosis the caspase-mediated cell death of human (LNCaP, DU145, and PC3) and mouse (HMVP2) prostate cancer cells (Zhang et al.,2019). NF-kB activity was downregulated by 6-Shogaol treatment with gamcetabine and gemcitabine-introduced activation of NF-κB was attenuated whereas gemcitabine and 6-shogaol got along. Expression of NF-κB-regulated gene products in tumor samples become additionally downregulated by using 6-shogaol. Inhibition of NF-κB signal is one in all the molecular mechanisms whereby 6-shogaol potentiates the antineoplastic action of gemcitabine. Immunohistochemistry disclosed large reduction of Ki-67 cells in tumors derived from mice handled with 6-shogaol and gemcitabine. However, the mix of the 2 become efficient (p<0>

Anti-biofilm property

6-shogaol exhibited anti-biofilm action by approach of inhibiting biofilm formation and removing the preformed biofilms of C. Auris (Candida Auris). The speed and extent of antibiofilm action are additionally confirmed by means that of a time-kill assay. The XTT reduction assay confirmed that 6-shogaol reduced cellular metabolic action within the biofilm. The result of 6-shogaol on initiated C. Auris biofilms became envisioned via confocal optical device scanning research. 6-shogaol attenuated the degrees of aspartyl proteinases and downregulated the expression of the effluence pump-related CDR1 factor in C. Auris (Kim et al., 2020). 6-Shogaol at 10µg/ml significantly reduced C. Albicans (Candida Albicans) biofilm formation however had no impact on organism cellular boom. Also, 6-Shogaol strangled hyphal increase in embedded colonies and loose-dwelling organism cells, and strangled cell aggregation (Lee et al., 2018).

Anti-viral property

6-Shogaol attenuated C. Albicans virulence in an exceedingly roundworm infection model while not inflicting toxicity at the examined concentrations. Transcriptomic analysis mistreatment RNA-seq and qRT-PCR confirmed 6-shogaol triggered many transporters (CDR1, CDR2, and RTA3), but inhibited the expressions of diverse filament associated genes (ECE1 and HWP1), that supported found phenotypical modifications. These effects spotlight the antivirulence activities of 6-shogaol, con to a drug resistant C. Albicans strain (Lee et al., 2018).

Conclusion

6-Shogaol is a compound that are widely used for many pharmacological purpose due to their beneficial activity. Most of the research indicated that it have highly anticancer activity also it show other important activity such as antioxidant, anti-inflammatory, antitumor, anti-biofilm and so on. Due to the beneficial activity of 6-shogaol this compound are under investigated. 

Conflicts of Interest

Not mentioned.

References

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