Protective effects of carnosic acid on retinal ganglion cells in acute ocular hypertension rats

Liang, Liang; He, Liye; Zhu, Mengnan; Chen, Baoji; Changyi, Xiao

doi:10.1007/s10792-020-01359-8

Cited by 4 publications

(4 citation statements)

References 20 publications

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“…However, these pathological processes were significantly inhibited by carnosic acid. Many studies have shown that the compound induces apoptosis in cancer cells [54] However, some studies have revealed the anti-apoptotic effect of carnosic acid on normal cells in inflammatory conditions [55][56][57][58][59]. In animal models of several inflammatory diseases, carnosic acid inhibited apoptosis to ameliorate inflammation and tissue injury [48,59,60].…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have shown that the compound induces apoptosis in cancer cells [54] However, some studies have revealed the anti-apoptotic effect of carnosic acid on normal cells in inflammatory conditions [55][56][57][58][59]. In animal models of several inflammatory diseases, carnosic acid inhibited apoptosis to ameliorate inflammation and tissue injury [48,59,60]. Thus, the cytoprotective effect of carnosic acid may contribute to its therapeutic action on LPS-induced AKI.…”

Section: Discussionmentioning

confidence: 99%

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Protective Effects of Carnosic Acid on Lipopolysaccharide-Induced Acute Kidney Injury in Mice

et al. 2021

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Septic acute kidney injury (AKI) is an important medical problem worldwide, but current treatments are limited. During sepsis, lipopolysaccharide (LPS) activates various signaling pathways involved in multiorgan failure. Carnosic acid is a natural phenolic diterpene and has multiple bioactivities, such as anti-tumor, anti-inflammatory, and anti-oxidative effects. However, the effect of carnosic acid on septic AKI has not been explored. Therefore, this study aimed to determine whether carnosic acid has a therapeutic effect on LPS-induced kidney injury. Administration of carnosic acid after LPS injection ameliorated histological abnormalities and renal dysfunction. Cytokine production, immune cell infiltration, and nuclear factor-κB activation after LPS injection were also alleviated by carnosic acid. The compound suppressed oxidative stress with the modulation of pro-oxidant and antioxidant enzymes. Tubular cell apoptosis and caspase-3 activation were also inhibited by carnosic acid. These data suggest that carnosic acid ameliorates LPS-induced AKI via inhibition of inflammation, oxidative stress, and apoptosis and could serve as a useful treatment agent for septic AKI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective Effects of Carnosic Acid on Lipopolysaccharide-Induced Acute Kidney Injury in Mice

et al. 2021

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“…Normal saline was infused into the centre of the anterior chamber for 60 min. No iris or lens injury was induced during the operation (22). At the indicated time point (day 1, 3, 7, 14 or 28), all the rats in each group were anesthetized with 3% sodium pentobarbital (30 mg/kg) and 3-5 ml of abdominal aortic blood was collected.…”

Section: Methodsmentioning

confidence: 99%

Neuroprotective role of epigallocatechin‑3‑gallate in acute glaucoma via the nuclear factor‑κB signalling pathway

et al. 2021

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Glaucoma is a disease involving impaired visual function accompanied by degeneration and necrosis of the optic nerve. Epigallocatechin-3-gallate (EGCG) exerts a neuroprotective effect against the degeneration of retinal ganglion cells. However, whether EGCG can relieve glaucoma and the possible mechanisms remain unclear. In order to determine the function of EGCG in glaucoma, an acute glaucoma rat model was established. Optic neuropathology was examined by haematoxylin-eosin staining and immunofluorescence staining for class III-β tubulin. The levels of inflammation-associated cytokines, such as interleukin (IL)-4, IL-6, TNF-α, IL-1β, IL-13 and IFN-γ were measured by flow cytometry. T cell proliferation was assessed by the carboxyfluorescein diacetate succinimidyl ester method. Finally, the functional role of EGCG in glaucoma was explored. The levels of the inflammation-associated proteins p-IκBα and p-p65 were measured by western blot analysis. The results showed that optic nerve injury occurred, and elevated levels of the inflammatory cytokines IL-4, IL-6, TNF-α, IL-1β, IL-13 and IFN-γ were observed in the rat model of acute glaucoma. In addition, an increased T lymphocyte proliferation rate and imbalance of Th1/Th2 cytokines were present in the models. Importantly, treatment with EGCG significantly alleviated optic nerve injury. At the molecular level, EGCG decreased the levels of inflammation-associated cytokines, decreased the proliferation rate of T lymphocyte cells, and repaired the imbalance of Th1/Th2 cytokines. Moreover, EGCG inhibited the increase in the phosphorylation of IκBα and p65 caused by modelling and thus suppressed the activation of the nuclear factor (NF)-κB signalling pathway. The findings of the present study indicate that EGCG could attenuate the symptoms of glaucoma and inhibit inflammatory responses by suppressing the NF-κB signalling pathway in a rat glaucoma model.

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“…In rats with acute ocular hypertension, CA also promoted protective effects on the oxidative damage of RGCs [ 307 ]. Finally, treatment of chlorpyrifos-intoxicated mice with CA (at 30 and 60 mg/kg/day for 14 days) markedly reduced the presence of MDA and NO in ocular and brain tissues and increased the non-enzymatic (GSH) and enzymatic (GPx, SOD, and CAT) antioxidant defences [ 308 ].…”

Section: Ca and Bcp: Therapeutic Potential In Eye-related Diseasesmentioning

confidence: 99%

Multi-Target Effects of ß-Caryophyllene and Carnosic Acid at the Crossroads of Mitochondrial Dysfunction and Neurodegeneration: From Oxidative Stress to Microglia-Mediated Neuroinflammation

2022

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Inflammation and oxidative stress are interlinked and interdependent processes involved in many chronic diseases, including neurodegeneration, diabetes, cardiovascular diseases, and cancer. Therefore, targeting inflammatory pathways may represent a potential therapeutic strategy. Emerging evidence indicates that many phytochemicals extracted from edible plants have the potential to ameliorate the disease phenotypes. In this scenario, ß-caryophyllene (BCP), a bicyclic sesquiterpene, and carnosic acid (CA), an ortho-diphenolic diterpene, were demonstrated to exhibit anti-inflammatory, and antioxidant activities, as well as neuroprotective and mitoprotective effects in different in vitro and in vivo models. BCP essentially promotes its effects by acting as a selective agonist and allosteric modulator of cannabinoid type-2 receptor (CB2R). CA is a pro-electrophilic compound that, in response to oxidation, is converted to its electrophilic form. This can interact and activate the Keap1/Nrf2/ARE transcription pathway, triggering the synthesis of endogenous antioxidant “phase 2” enzymes. However, given the nature of its chemical structure, CA also exhibits direct antioxidant effects. BCP and CA can readily cross the BBB and accumulate in brain regions, giving rise to neuroprotective effects by preventing mitochondrial dysfunction and inhibiting activated microglia, substantially through the activation of pro-survival signalling pathways, including regulation of apoptosis and autophagy, and molecular mechanisms related to mitochondrial quality control. Findings from different in vitro/in vivo experimental models of Parkinson’s disease and Alzheimer’s disease reported the beneficial effects of both compounds, suggesting that their use in treatments may be a promising strategy in the management of neurodegenerative diseases aimed at maintaining mitochondrial homeostasis and ameliorating glia-mediated neuroinflammation.

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Protective effects of carnosic acid on retinal ganglion cells in acute ocular hypertension rats

Cited by 4 publications

References 20 publications

Protective Effects of Carnosic Acid on Lipopolysaccharide-Induced Acute Kidney Injury in Mice

Protective Effects of Carnosic Acid on Lipopolysaccharide-Induced Acute Kidney Injury in Mice

Neuroprotective role of epigallocatechin‑3‑gallate in acute glaucoma via the nuclear factor‑κB signalling pathway

Multi-Target Effects of ß-Caryophyllene and Carnosic Acid at the Crossroads of Mitochondrial Dysfunction and Neurodegeneration: From Oxidative Stress to Microglia-Mediated Neuroinflammation

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