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Nirmala, Chandrasekar; Anand, Selvaraj; Puvanakrishnan, Rengarajulu

doi:10.1023/a:1006960106929

Cited by 25 publications

(4 citation statements)

References 32 publications

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“…Myocardial edema, necrosis, and inflammatory cells are the reasons for the cardiac hypertrophy observed in myocardial infarcted rats. [ 26 ] Administration of β‐caryophyllene repressed the occurrence of cardiac hypertrophy in myocardial infarcted rats, by its anti‐cardiac hypertrophic effect.…”

Section: Discussionmentioning

confidence: 99%

β‐Caryophyllene inhibits Fas‐ receptor and caspase‐mediated apoptosis signaling pathway and endothelial dysfunction in experimental myocardial infarction

Yovas

Ponnian

2021

J Biochem & Molecular Tox

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We planned to appraise the effects of β‐caryophyllene on Fas‐ receptor and caspase‐mediated apoptosis signaling pathway and endothelial dysfunction in rats infarcted with isoproterenol. Rats were induced myocardial infarction by using isoproterenol (100 mg/kg body weight [b.w]). Serum creatine kinase‐MB, serum cardiac troponin‐T, heart weight, heart rate, and heart lipid peroxidation were greatly (p < 0.05) augmented, while heart enzymatic antioxidants and plasma nonenzymatic antioxidants were greatly (p < 0.05) lessened in isoproterenol‐treated rats. Reverse transcription‐polymerase chain reaction study revealed augmented expressions of Fas‐receptor and caspases 8, 9, and 3 genes in myocardial infarcted rats. Furthermore, iNOS protein expression was amplified and eNOS protein was lessened in the myocardial infarcted heart. Three weeks pre‐ and cotreatment with β‐caryophyllene (20 mg/kg b.w) greatly (p < 0.05) protected isoproterenol‐treated rats against these altered structural, biochemical, molecular, and immunohistochemical parameters, by its anti‐cardiac hypertrophic, anti‐tachycardial, antioxidant, anti‐apoptotic, and anti‐endothelial dysfunction effects. In conclusion, these findings projected the use of β‐caryophyllene for the therapy of human myocardial infarction after clinical trials.

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Section: Discussionmentioning

confidence: 99%

β‐Caryophyllene inhibits Fas‐ receptor and caspase‐mediated apoptosis signaling pathway and endothelial dysfunction in experimental myocardial infarction

Yovas

Ponnian

2021

J Biochem & Molecular Tox

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“…Curcumin has also proven its efficacy in protecting rat myocardium from myocardial ischemic injury induced by isoprenaline (Nirmala and Puvanakrishnan, 1996; Manikandan et al, 2004). These beneficial effects of curcumin were mainly associated with its ability in ROS scavenging and the inhibition of lysosomal enzymes (Nirmala et al, 1999). Treatment with curcumin also exhibited beneficial effects in kidney damage by limiting the expression of Fas-L and Fas (Jones et al, 2000).…”

Section: Other Potential Effects Of Curcuminmentioning

confidence: 99%

Curcumin as an Alternative Epigenetic Modulator: Mechanism of Action and Potential Effects

et al. 2019

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Curcumin (a polyphenolic compound in turmeric) is famous for its potent anti-inflammatory, anti-oxidant, and anti-cancer properties, and has a great potential to act as an epigenetic modulator. The epigenetic regulatory roles of curcumin include the inhibition of DNA methyltransferases (DNMTs), regulation of histone modifications via the regulation of histone acetyltransferases (HATs) and histone deacetylases (HDACs), regulation of microRNAs (miRNA), action as a DNA binding agent and interaction with transcription factors. These mechanisms are interconnected and play a vital role in tumor progression. The recent research has demonstrated the role of epigenetic inactivation of pivotal genes that regulate human pathologies such as cancers. Epigenetics helps to understand the mechanism of chemoprevention of cancer through different therapeutic agents. In this regard, dietary phytochemicals, such as curcumin, have emerged as a potential source to reverse epigenetic modifications and efficiently regulate the expression of genes and molecular targets that are involved in the promotion of tumorigenesis. The curcumin may also act as an epigenetic regulator in neurological disorders, inflammation, and diabetes. Moreover, curcumin can induce the modifications of histones (acetylation/deacetylation), which are among the most important epigenetic changes responsible for altered expression of genes leading to modulating the risks of cancers. Curcumin is an effective medicinal agent, as it regulates several important molecular signaling pathways that modulate survival, govern anti-oxidative properties like nuclear factor E2-related factor 2 (Nrf2) and inflammation pathways, e.g., nuclear factor kappa B (NF-κB). Curcumin is a potent proteasome inhibitor that increases p-53 level and induces apoptosis through caspase activation. Moreover, the disruption of 26S proteasome activity induced by curcumin through inhibiting DYRK2 in different cancerous cells resulting in the inhibition of cell proliferation opens up a new horizon for using curcumin as a potential preventive and treatment approach in proteasome-linked cancers. This review presents a brief summary of knowledge about the mechanism of epigenetic changes induced by curcumin and the potential effects of curcumin such as anti-oxidant activity, enhancement of wound healing, modulation of angiogenesis and its interaction with inflammatory cytokines. The development of curcumin as a clinical molecule for successful chemo-prevention and alternate therapeutic approach needs further mechanistic insights.

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“…Bleomycin treatment significantly increased the HYP content of the lung by generating free radicals (20) while curcumin blocked the formation of toxic free radicals, which in turn could significantly decrease HYP production. Also, curcumin can modulate collagen metabolism (21). Unlike oral curcumin administration and curcumin inhalation, our data showed that the inhalation of the synthesized nano-curcumin could restore lung HYP content.…”

Section: Discussionmentioning

confidence: 80%

The Protective Effects of Nebulized Nano-Curcumin Against Bleomycin-Induced Pulmonary Fibrosis in Rats

Hemmati

Karampour

Dahanzadeh

et al. 2021

Jundishapur J Nat Pharm Prod

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Background: Idiopathic pulmonary fibrosis (IPF) is a progressive fatal disease affecting the lung, and currently there is no efficient therapy for this condition. Curcumin, as a natural anti-inflammatory and antioxidant agent, could repress the pulmonary fibrosis (PF) caused by Bleomycin (BLM). Objectives: The aim of the research was to evaluate the protective activity of a nano-formulation of curcumin administered by inhalation on BLM-induced PF in rats. Methods: Eighty rats were randomly divided into eight experimental groups. Group one (control) that received saline intratracheally (IT) and subjected to vehicle inhalation. Group two to eight each received a single dose of BLM (5 IU/kg, IT) along with vehicle inhalation, oral prednisolone, oral curcumin, curcumin inhalation, and nano-curcumin inhalation with the doses of 50, 100, and 200 µg/kg, respectively. In the control and other groups, BLM was injected intratracheally on the first day of the experiment. In the treatment groups, curcumin suspension was prepared in distilled water and applied through nebulization for 21 consecutive days after BLM intratracheal administration. Then the rats were euthanized, and inflammatory cytokines (TNF-α, TGF-β, PDGF), hydroxyproline, and IL-10 (as a protective cytokine) were measured. Also, lung histopathological features were examined. Results: The synthesized nano-formulation reduced the overall hydroxyproline content of lungs in BLM-treated rats (P < 0.002). In addition, TNF-α, TGF-β, and PDGF levels significantly increased in the lungs of BLM-instilled rats (P < 0.001). However, the nano-formulation of curcumin (200 µg/kg) significantly decreased the levels of these inflammatory cytokines (P < 0.001) and increased IL-10 level (P = 0.0144) compared with the control group. Conclusions: The nebulization of nano-curcumin is suggested as a novel approach for the treatment of PF induced by BLM in rats. Our findings revealed that the inhalation (as a safe local drug delivery system approach) of the nano-curcumin at a dose of 200 µg/kg (formulated by cyclodextrin) could effectively protect the lung against PF.

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Cited by 25 publications

References 32 publications

β‐Caryophyllene inhibits Fas‐ receptor and caspase‐mediated apoptosis signaling pathway and endothelial dysfunction in experimental myocardial infarction

β‐Caryophyllene inhibits Fas‐ receptor and caspase‐mediated apoptosis signaling pathway and endothelial dysfunction in experimental myocardial infarction

Curcumin as an Alternative Epigenetic Modulator: Mechanism of Action and Potential Effects

The Protective Effects of Nebulized Nano-Curcumin Against Bleomycin-Induced Pulmonary Fibrosis in Rats

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