CD147 Protein Expression and Temozolomide Resistance in Glioma Cells: An Ex vivo and In vivo Study.

It has been noted that temozolomide resistance occurs in a number of malignancies, including glioma, although the underlying cause of this is unknown. The goal of the study in vivo investigation to show that increased CD147 expression in glioma cells is a factor in their resistance to the chemotherapy drug temozolomide. Proliferation assays, TUNEL assays, reactive oxygen species assays, protein degradation assays, immunohistochemistry, Western blotting, quantitative polymerase chain reactions, and tumorigenicity assays were all carried out. Using the human protein atlas databases, the expression levels of CD147 in different kinds of malignancies were examined. For immunohistochemistry, a total of 7, 12, 19, 15, and 16 glioma samples were taken from para-carcinoma tissue, representing stage I, stage II, stage III, and stage IV gliomas, respectively. The expression of CD147 proteins is correlated with the tumor's aggressiveness. Cell development was slowed by suppressing the expression of the CD147 protein. The expression of the CD147 protein contributed to the emergence of temozolomide resistance. Expression of the CD147 protein reduced mRNA expression. The growth-inhibitory impact of temozolomide on glioma cells was enhanced by the suppression of CD147 protein.  Nuclear factor E2-related factor 2 expression and CD147 protein expression showed a significant reciprocal connection with each other (p 0.0001, r2 = 0.3254). In glioma, resistance to temozolomide is due to overexpression of CD147 protein and induction of nuclear factor E2-related factor 2.

Anthocyanin can arrest the cone photoreceptor degeneration and act as a novel treatment for retinitis pigmentosa.

Retinitis pigmentosa (RP) is a group of heterogeneous inherited retinal diseases that is characterized by primary death rod photoreceptors and the secondary loss of cones. The degeneration of cones causes gradual constriction of visual fields, leaving the central islands that are eventually snuffed out. Studies indicate that the hyperoxia causes oxidative damage in the retina and contributes to the cone death of RP. Moreover, abundant reactive oxidative species (ROS) which are generated in cones may result in mitochondria membrane depolarization, which has been ascribed a central role in the apoptotic process and has been proposed to act as a forward feeding loop for the activation of downstream cascades. Anthocyanin is a potent antioxidant which has been evidenced to be able to counteract oxidative damages, scavenge surplus ROS, and rectify abnormities in the apoptotic cascade. Taken together with its ability to attenuate inflammation which also contributes to the etiology of RP, it is reasonable to hypothesize that the anthocyanin could act as a novel therapeutic strategy to retard or prevent cone degeneration in RP retinas, particularly if the treatment is timed appropriately and delivered efficiently. Future pharmacological investigations will identify the anthocyanin as an effective candidate for PR therapy and refinements of that knowledge would ignite the hope of restoring the visual function in RP patients.

The transcorneal electrical stimulation as a novel therapeutic strategy against retinal and optic neuropathy: a review of experimental and clinical trials.

Transcorneal electrical stimulation (TES) is a novel therapeutic approach to activate the retina and related downstream structures. TES has multiple advantages over traditional treatments, such as being minimally invasive and readily applicable in a routine manner. Series of animal experiments have shown that TES protects the retinal neuron from traumatic or genetic induced degeneration. These laboratory evidences support its utilization in ophthalmological therapies against various retinal and optical diseases including retinitis pigmentosa (RP), traumatic optic neuropathy, anterior ischemic optic neuropathy (AION), and retinal artery occlusions (RAOs). Several pioneering explorations sought to clarify the functional mechanism underlying the neuroprotective effects of TES. It seems that the neuroprotective effects should not be attributed to a solitary pathway, on the contrary, multiple mechanisms might contribute collectively to maintain cellular homeostasis and promote cell survival in the retina. More precise evaluations via functional and morphological techniques would determine the exact mechanism underlying the remarkable neuroprotective effect of TES. Further studies to determine the optimal parameters and the long-term stability of TES are crucial to justify the clinical significance and to establish TES as a popularized therapeutic modality against retinal and optic neuropathy.