Amelioration of Aluminum Maltolate-Induced Inflammation and Endoplasmic Reticulum Stress-Mediated Apoptosis by Tannoid Principles of Emblica officinalis in Neuronal Cellular Model

Bharathi, Mathiyazahan Dhivya; Justin-Thenmozhi, Arokiasamy; Manivasagam, Thamilarasan; Rather, Mashoque Ahmad; Babu, Chidambaram Saravana; Essa, Musthafa Mohamed; Guillemin, Gilles J.

doi:10.1007/s12640-018-9956-5

Cited by 28 publications

(6 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In several experimental models of hepatic fibrosis, those proinflammatory mediators are regarded as the major hepatotoxic mediators which mainly contribute to HSC activation and ECM generation [ 34 , 45 ]. Some reports stated that various extracts from PE cause inhibition of the production of TNF- α , IL-1 β, and IL-6 in atherosclerosis or neuronal cellular model [ 46 , 47 ]. Overall, the data from the present study have shown that AEPE exerts a protective effect on liver cells by reducing the level of inflammatory factors, which were consistent with the inflammatory cell infiltration found in H&E staining.…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective Effect and Potential Mechanism of Aqueous Extract from Phyllanthus emblica on Carbon-Tetrachloride-Induced Liver Fibrosis in Rats

Yin

Luo

et al. 2021

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Liver fibrosis is a pathological variation caused by almost all chronic liver injuries. As an edible and medicinal natural resource, Phyllanthus emblica (PE) has been reported to possess hepatoprotective, antioxidant, and anti-inflammatory activities and may have an ameliorating effect on hepatic fibrosis. To investigate the protective effect of the aqueous extract of PE (AEPE) against liver fibrosis and to uncover its related mechanisms, the chemical profile of AEPE was characterized by high performance liquid chromatography (HPLC) and sulfuric acid-phenol method. Ameliorative effects of different doses of AEPE were investigated in carbon-tetrachloride- (CCl4-) induced liver fibrosis rats by analyzing biochemical markers, morphologic pathology, and related proteins expression in liver tissue. The results indicated that AEPE (1.8, 3.6 g/kg) could significantly reduce levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), collagen IV (Col IV), type III precollagen (PCIII), hyaluronic acid (HA), laminin (LN), malondialdehyde (MDA), nitric oxide (NO), protein carbonyl (PC), tumor necrosis factor-α(TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and hydroxyproline (Hyp) and increase the levels of superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT). Hematoxylin-eosin (H&E), Sirius red, and Masson staining showed AEPE-treated improved fibrotic lesions and inflammatory cell infiltration. Meanwhile, AEPE treatment also significantly downregulates the expression of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) in the liver tissue and serum, respectively. In conclusion, AEPE possesses curative efficacy against liver fibrosis through its antioxidant, anti-inflammatory, and antifibrotic effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Hepatoprotective Effect and Potential Mechanism of Aqueous Extract from Phyllanthus emblica on Carbon-Tetrachloride-Induced Liver Fibrosis in Rats

Yin

Luo

et al. 2021

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

show abstract

“…The roles played by HMGB1 in regulating ER stress and ROS production have also been well documented. Cells exposed to external or internal stress release a series of damage-associated molecular patterns (DAMPs), including HMGB1; this release mediates an inflammatory response, ER stress, and ROS synthesis 18. Recent studies have shown that HMGB1 might affect the tumorigenesis of cancers by interacting with miRNAs 34,35.…”

Section: Discussionmentioning

confidence: 99%

“…HMGB1 was previously reported to participate in the pathogenesis of various human diseases, such as sepsis,16 and cancers,17 by interacting with miRNAs. During ER stress, neurons could release HMGB1 to trigger the initiation of neuron-inflammation and glial activation.18 As for cancer research, HMGB1 has been demonstrated as an oncogene inhibiting cell apoptosis through mediating ER stress,19 accompanying with reactive oxygen species (ROS) production.20 A recent study suggested that ROS induction can lead to cell apoptosis and exert a anti-drug-resistance effect on lung cancer.21 This might be due to the occurrence of DNA damage in lung cancer induced by ROS generation through mitochondrial membrane potential reprogramming.22–24…”

Section: Introductionmentioning

confidence: 99%

<p>MiR-34c acts as a tumor suppressor in non-small cell lung cancer by inducing endoplasmic reticulum stress through targeting HMGB1</p>

Long

Song

et al. 2019

OTT

View full text Add to dashboard Cite

Objective To investigate the role of miR-34c in lung cancer. Methods The levels of microRNA-34c (miR-34c) expression in non-small cell lung cancer (NSCLC) tissue and cell lines were examined by the qRT-PCR assay. High mobility group box 1 (HMGB1) expression in NSCLC was assessed by immunohistochemical analysis (IHC), qRT-PCR, and Western blot assays. The effects of miR-34c overexpression or HMGB1 knockdown on cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. Cellular reactive oxygen species (ROS) production in NSCLC cells was detected using a ROS kit. The levels of Bax, p-ERK, eIF2α, GADD153, and IRE1α expression in treated NSCLC cells were measured by Western blot assays. In addition, the interaction between miR-34c and HMGB1 was verified by the dual-luciferase reporter assay. Results miR-34c was only slightly expressed, while HMGB1 was highly expressed in NSCLC tissues and cell lines. Overexpression of miR-34c or knockdown of HMGB1 inhibited cell proliferation, promoted cell apoptosis, and induced ER stress in NSCLC cells. In terms of mechanism, miR-34c negatively regulated HMGB1 expression by directly targeting the 3ʹ-untranslated region (UTR) of HMGB1 mRNA. In addition, we proved that HMGB1 overexpression could block the effects of miR-34c on NSCLC cell proliferation, apoptosis, and ER stress. Conclusion miR-34c may suppress NSCLC tumors by targeting HMGB1 mRNA, promoting endoplasmic reticulum stress, and increasing ROS levels. Our findings suggest that miR-34c has a role in NSCLC.

show abstract

“…Neuronal apoptosis plays an important role in neurodegenerative diseases, such as AD, which can lead to the loss of a large number of neurons ( Bredesen, 1995 ; Caccamo et al, 2017 ). It is influenced by Aβ, Bcl-2-associated X protein (Bax), Bcl2, caspases, TNF-α, ROS, and enzyme perturbation ( Dhivya Bharathi et al, 2019 ). The mechanisms of neuronal apoptosis include the following: 1) the extrinsic pathway, initiated by cell surface death receptors such as Fas and tumor necrosis factor receptor families; 2) the intrinsic pathway or mitochondrial pathway, initiated by stress conditions, chemotherapeutic agents, and drugs; and 3) activation of caspase 12 caused by endoplasmic reticulum stress, leading to apoptosis ( Boatright and Salvesen, 2003 ).…”

Section: Anti-ad Effects Of Erigeron Breviscapus (...mentioning

confidence: 99%

Erigeron breviscapus (Vant.) Hand-Mazz.: A Promising Natural Neuroprotective Agent for Alzheimer’s Disease

Dong

2022

Front. Pharmacol.

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is the most common neurodegenerative disease and is characterized by progressive cognitive dysfunction and memory loss in the elderly, which seriously affects the quality of their lives. Currently, the pathogenesis of AD remains unclear. Molecular biologists have proposed a variety of hypotheses, including the amyloid-β hypothesis, tau hyperphosphorylation hypothesis, cholinergic neuron injury, inflammation caused by an abnormal immune response, and gene mutation. Drugs based on these pathological studies, including cholinesterase inhibitors and N-methyl-D-aspartate receptor antagonists, have achieved a certain level of efficacy but are far from meeting clinical needs. In the recent years, some important advances have been made in the traditional Chinese medicine treatment of AD. Erigeron breviscapus (Vant.) Hand-Mazz. (EBHM) is an important medicinal plant distributed in Yunnan Province, China. Studies have shown that EBHM and its active ingredients have a variety of pharmacological effects with good therapeutic effects and wide application prospects for cognitive disability-related diseases. However, to our best knowledge, only few review articles have been published on the anti-AD effects of EBHM. Through a literature review, we identified the possible pathogenesis of AD, discussed the cultivation and phytochemistry of EBHM, and summarized the pharmacological mechanism of EBHM and its active ingredients in the treatment of AD to provide suggestions regarding anti-AD therapy as well as a broader insight into the therapeutic potential of EBHM.

show abstract

Amelioration of Aluminum Maltolate-Induced Inflammation and Endoplasmic Reticulum Stress-Mediated Apoptosis by Tannoid Principles of Emblica officinalis in Neuronal Cellular Model

Cited by 28 publications

References 48 publications

Hepatoprotective Effect and Potential Mechanism of Aqueous Extract from Phyllanthus emblica on Carbon-Tetrachloride-Induced Liver Fibrosis in Rats

Hepatoprotective Effect and Potential Mechanism of Aqueous Extract from Phyllanthus emblica on Carbon-Tetrachloride-Induced Liver Fibrosis in Rats

<p>MiR-34c acts as a tumor suppressor in non-small cell lung cancer by inducing endoplasmic reticulum stress through targeting HMGB1</p>

Erigeron breviscapus (Vant.) Hand-Mazz.: A Promising Natural Neuroprotective Agent for Alzheimer’s Disease

Contact Info

Product

Resources

About