The mechanism of UVB irradiation induced-apoptosis in cataract

Ji, Yinghong; Cai, Lei; Zheng, Tianyu; Ye, Hongfei; Xiao, Rong; Rao, Jun; Lü, Yi

doi:10.1007/s11010-014-2294-x

Cited by 61 publications

(58 citation statements)

References 33 publications

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“…Previous studies have shown that UVB irradiation could efficiently induce HLECs apoptosis in a time and dose dependent manner [2]. The annexin V-FITC/propidium iodide (PI) staining results revealed that the percentage of primary apoptotic cells in CRTAC1 interfe-rence group was fewer than those in model group and empty vector group (Fig.…”

Section: Inhibition Of Crtac1 Expression Reduced Uvb Irradiation Indumentioning

confidence: 87%

“…For apoptosis detection, the HLECs were collected and incubated in 5 µL annexin buffer and 5 µL propidium iodide (PI) for 10 min; for ROS detection, the HLECs were incubated with culture medium containing 10 µM DCFH-DA for 30 min; and the HLECs were incubated with Fluo-3 (10 µM, Sigma) for 30 min for determination of intracellular calcium concentration. Additionally, the level of ∆Ψm in HLECs was measured using cationic dye JC-1 assay kit as our previous study [2].…”

Section: Flow Cytometry Analysis Of Apoptosis Ros Production Calciumentioning

confidence: 99%

“…Cataract is one of the most common eye diseases and can eventually lead to blindness [1,2]. It is believed that cataract can be caused by some major risk factors including aging, UVB irradiation and hydrogen peroxide (H 2 O 2 ) [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

“…Bax expression is increased but Bcl-2 expression is decreased during UVB-induced apoptosis in cataract, suggesting both proteins play pivotal roles in cataract formation [2]. Experimental and clinical evidences have indicated that mitogen activated protein kinase (MAPK) signal pathway plays a key role in regulating cell apoptosis [20].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Xiao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Ultraviolet B (UVB) irradiation can easily induce apoptosis in human lens epithelial cells (HLECs) and further lead to various eye diseases including cataract. Here for the first time, we investigated the role of cartilage acidic protein 1 (CRTAC1) gene in UVB irradiation induced-apoptosis in HLECs. Methods: Three groups of HLECs were employed including model group, empty vector group, and CRTAC1 interference group. Results: After UVB irradiation, the percentage of primary apoptotic cells was obviously fewer in CRTAC1 interference group. Meanwhile, inhibition of CRTAC1 also reduced both reactive oxygen species (ROS) production and intracellular Ca²⁺ concentration, but the level of mitochondrial membrane potential (Δψm) was increased in HLECs. Further studies indicated that superoxide dismutase (SOD) activity and total antioxidative (T-AOC) level were significantly increased in CRTAC1-inhibited cells, while the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) were significantly decreased. ELISA analysis of CRTAC1-inhibited cells showed that the concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly decreased, but the concentration of interleukin-10 (IL-10) was significantly increased. Western blot analyses of eight apoptosis-associated proteins including Bax, Bcl-2, p38, phospho-p38 (p-p38), Jun amino-terminal kinases (JNK1/2), phospho-JNK1/2 (p-JNK1/2), calcium-sensing receptor (CasR), and Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) indicated that the inhibition of CRTAC1 alleviated oxidative stress and inflammation response, inactivated calcium-signaling pathway, p38 and JNK1/2 signal pathways, and eventually reduced UVB irradiation induced-apoptosis in HLECs. Conclusion: These results provided new insights into the mechanism of cataract development, and demonstrated that CRTAC1 could be a potentially novel target for cataract treatment.

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Section: Inhibition Of Crtac1 Expression Reduced Uvb Irradiation Indumentioning

confidence: 87%

Section: Flow Cytometry Analysis Of Apoptosis Ros Production Calciumentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Xiao

et al. 2016

Cell Physiol Biochem

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“…SD rats were subjected to UV irradiation model construction according to the methods described by Ji et al (9). Rats were randomly divided into 2 groups including control group (n=12) and model group (n=48).…”

Section: Methodsmentioning

confidence: 99%

Effects of UV on apoptotic factors in lens epithelial cells of an animal model

Xing

2018

Exp Ther Med

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Effect of ultraviolet (UV) on the apoptotic factors p53, Bax and Bcl-2 in lens epithelial cells (LECs) was explored. Sixty SD rats were randomly divided into control group (n=12) and model group (n=48). Rats in model group were used to construct UV radiation eyeball models. Twelve rats in model group and 3 rats in control group were sacrificed at day 1, 3, 5 and 7, and the expression of p53, Bax and Bcl-2 in LECs was detected by RT-qPCR. There was no significant difference in p53 expression between model and control group on day 1 (P>0.05), while expression level of p53 was significantly higher in model than in control group at day 3, 5 and 7 (P<0.05), and the highest expression level was found on day 7 (P<0.05). Relative expression level of Bax in model group was significantly higher than that in control group (P<0.05), and the highest expression level was found on day 7 (P<0.05). On day 1, expression level of Bcl-2 in model group was significantly lower than that in control group (P<0.05), but it began to rise on day 3 but did not differ significantly from the control group (P>0.05), and was significantly higher in model than in control group on day 5 and 7 (P<0.05), and the highest expression level was observed on day 7 (P<0.05). Linear correlation analysis showed that there was a positive correlation between p53, Bax and Bcl-2 expression and UV exposure time in LEC (r=0.82, 0.90, 0.95, P<0.05). Expression levels of p53, Bax, and Bcl-2 in LEC of rats are positively correlated with the time after UV irradiation, suggesting that UV could induce apoptosis of LEC by promoting p53, Bax and Bcl-2 expression.

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Impact of chrysin on the molecular mechanisms underlying diabetic complications

Farkhondeh

Samarghandian

Roshanravan

2019

Journal Cellular Physiology

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Diabetes mellitus is a chronic metabolic disorder, resulting in high morbidity and mortality worldwide. Neuropathy, ocular diseases, kidney diseases, and cardiovascular disease are common complications of diabetes that threats the patient’s life. Chrysin (CH), a natural flavonoid, has several pharmacological effects, including antioxidant, antiapoptotic, anti‐inflammatory, and anticancer. Strong scientific documents indicated that chrysin may be effective for preventing and treating complications of diabetes in experimental models. The present study was designed to review the association between chrysin administration and diabetes complications by focusing on the possible molecular pathway. The findings indicate that chrysin has protective effects against diabetes outcomes by modulating oxidative stress, inflammation, and apoptosis in animal models. However, more clinical trial study should be done to clear the protective effects of chrysin in diabetic patients.

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The mechanism of UVB irradiation induced-apoptosis in cataract

Cited by 61 publications

References 33 publications

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Effects of UV on apoptotic factors in lens epithelial cells of an animal model

Impact of chrysin on the molecular mechanisms underlying diabetic complications

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