Hispolon inhibits RANKL induced osteoclast differentiation in vitro

Thimmuri, Dinesh; Shantanu, P. A.; Syamprasad, N P; Khan, Aasiya; Gawali, Basveshwar; Rajdev, Bishal; Adhikari, Chanakya; Ravichandiran, V.; Sharma, Pawan; Naidu, V.G.M.

doi:10.1016/j.imlet.2021.01.003

Cited by 6 publications

(3 citation statements)

References 26 publications

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“…Importantly, the OPG/RANKL/RANK axis regulates osteoblast and osteoclast formation, indicated by expression of ALP and RUNX2, or CTSK and TRAP, respectively. 32,46,47 ALP is a biomarker indicating the differentiation of osteoblast progenitor cells into mature osteoblasts, and is regulated by the transcription factor RUNX2. 48 Mice deficient in Runx2 in the bone (encoding RUNX2) display endochondral defects and defects in intramembranous formation.…”

Section: Discussionmentioning

confidence: 99%

Puerarin alleviates cadmium‐induced oxidative damage to bone by reducing autophagy in rats

Tong

Guo

Liu

et al. 2021

Environmental Toxicology

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Autophagy is a regulatory mechanism involved in cadmium (Cd)-induced bone toxicity and is suppressed by various stimuli, including oxidative stress. Puerarin is an isoflavonoid compound isolated from Pueraria, a plant used in traditional Chinese medicine. The underlying mechanisms of action of puerarin remain unclear. The objective of this study was to explore the mitigating effects of puerarin on cadmiuminduced oxidative damage in the bones of rats. Cadmium exposure increased oxidative damage in rat bones; this was markedly decreased by puerarin treatment, as demonstrated by changes in the activity of antioxidative enzymes. Cadmium-induced blockage of the expression of key bone regulatory proteins, autophagy-related markers, and signaling molecules was also alleviated by puerarin treatment. Additionally, cadmium reduced expression of the autophagic protein Rab7 and of late endosomal/lysosomal adaptor and MAPK and mTOR activator 1 (LAMTOR1); the decrease in these proteins was not restored by puerarin treatment. We speculate that puerarin relieves the inhibition of fusion of autophagosomes with lysosomes that is induced by cadmium; however, this specific effect of puerarin and downstream effects on bone regulatory mechanisms require further investigation. In conclusion, puerarin alleviates cadmium-induced oxidative damage in the bones of rats by attenuating autophagy, which is likely associated with the antioxidant activity of puerarin.

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Section: Discussionmentioning

confidence: 99%

Puerarin alleviates cadmium‐induced oxidative damage to bone by reducing autophagy in rats

Tong

Guo

Liu

et al. 2021

Environmental Toxicology

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“…Later, it was incubated with uorescent conjugated secondary antibodies (Alexa Flour 488 and 594), washed, and mounted with a DAPI -gold antifade mounting medium. Further images were acquired using confocal microscopy (Leica TCS SP-8) [24].…”

Section: Immuno Uorescencementioning

confidence: 99%

AKR1B1 drives hyperglycemia-induced metabolic reprogramming in NAFLD-associated carcinogenesis and progression of hepatocellular carcinoma

Jain

Rajdev

et al. 2023

Preprint

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Objective Emergent epidemiological evidence suggests that the progression of NAFLD/NASH-associated HCC positively correlates with the patient's glycemic index. However, the mechanism behind this progressive pathological alteration is poorly understood. It has shown that the polyol pathway master regulator, AKR1B1 is over-expressed in hyperglycemia and responsible for most of diabetic complications. Hence in the present study, we have investigated the role of AKR1B1 in metabolic switching associated with NAFLD/NASH and in the progression of HCC. Methods The expression of AKR1B1 in NAFL/NASH, HCC, and HCC with diabetes mellitus patient's liver and plasma were estimated. The role of AKR1B1 in the metabolic switching of HCC cell lines was assessed through media conditioning and lentiviral transfection. Standard inhibitor epalrestat or investigational drug NARI-29 (4-((Z)-5-((Z)-2-Cyano-3-phenylallylidene)-4-oxo-2-thioxothiazolidin-3-yl) benzoic acid) was utilized to elucidate the effect of AKR1B1 inhibition in hepatocarcinogenesis. A proteomic approach was applied for an in-depth investigation of the involved metabolic pathway and to evaluate the therapeutic efficacy of pharmacological inhibitors. Preclinically, a high fructose diet (HFrD) fed in combination with a diethyl nitrosamine (DEN) induced mouse model was developed to investigate the role of AKR1B1 in the hyperglycemia-mediated metabolic switching in the pathobiology of NAFLD and its progression to HCC. Results A significant increase in the expression of AKR1B1 was observed in NAFL/NASH, HCC, and HCC-DM tissue samples compared to non-involved adjacent tissues indicating its role in the disease progression. Moreover, a statistically significant elevation of AKR1B1 was observed in NAFLD, NAFLD-associated HCC, and HCC-DM plasma samples compared to normal control. Mechanistically, Invitro assays revealed that AKR1B1 modulates the Warburg effect, mitochondrial dynamics, TCA cycle, and lipogenesis to promote hyperglycemia-mediated fatty liver and cancer progression. A pathologically increased expression of AKR1B1 was observed in experimental NAFL-HCC, and expression was positively correlated with high blood glucose levels. HFrD + DEN-treated animals also exhibited statistically significant elevation of metabolic markers and carcinogenesis markers. However, AKR1B1 inhibition with EPS or NARI-29 has inhibited cellular metabolism in vitro and in vivo models. Conclusion Pathological AKR1B1 modulates hepatic glucose metabolism to promote NAFLD-associated hepato-carcinogenesis. Aldose reductase inhibition modulates glucose metabolism to prevent the pre-cancerous hepatocyte formation. Hence EPS and NARI-29 could be promising AKR1B1 inhibitors for controlling aberrant metabolism and treating NAFLD-associated HCC.

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“…Cooperatively, these metabolites may be a novel source of protecting agents against neurodegenerative conditions. Thimmuri et al 44 first time reported the anti-osteoclastogenic effect of hispolon and revealed its mechanism of action. Hispolonreduced the RANKL expression that persuaded the differentiation of RAW 264.7 into osteoclasts, further downregulated the activation of NFkB and MAP kinase pathway.…”

Section: Antioxidative and Cytoprotectivementioning

confidence: 99%

Biological Activities of Hispolon

Kolla¹,

Bollikolla²

2022

CJST

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Natural products are a great source for the discovery of new chemotherapeutic agents. Phenolic compounds are significant natural products, mostly from the source of microorganisms and plants. Among fungi, mushrooms are not only the source of nutrients but also many bioactive components. In this paper, the authors made a comprehensive review of the biological activities of hispolon. The biological activities like anticancer, antioxidant, anti-inflammatory, and antimicrobial are possessed by hispolon. Along with anti-tuberculosis properties, hispolon exhibited effectiveness in the treatment of metabolic disorders and functional as immunomodulators.

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Hispolon inhibits RANKL induced osteoclast differentiation in vitro

Cited by 6 publications

References 26 publications

Puerarin alleviates cadmium‐induced oxidative damage to bone by reducing autophagy in rats

Puerarin alleviates cadmium‐induced oxidative damage to bone by reducing autophagy in rats

AKR1B1 drives hyperglycemia-induced metabolic reprogramming in NAFLD-associated carcinogenesis and progression of hepatocellular carcinoma

Biological Activities of Hispolon

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