@article {2409, title = {The Effects of Melon Superoxide Dismutase and Gliadin on Glutathione Reductase (GSH) and Superoxide Dismutase (SOD) Levels in Blood Plasma and Vitreoretina in Diabetic Rat Model: A Literature Review}, journal = {Pharmacognosy Journal}, volume = {16}, year = {2024}, month = {October 2024}, pages = {1202-1208}, type = {Review Article}, chapter = {1202}, abstract = {

Chronic hyperglycemia in diabetics causes microvascular damage through four mechanisms of biochemical changes, including activated protein kinase C (PKC) pathway, activated hexosamine pathway, increased polyol pathway, and increased advanced glycation end-products (AGEs), all of which will increase Reactive Oxygen Species (ROS) levels. ROS can damage proteins, nucleic acids, and lipids and hasten the onset of diabetes. ROS are produced in the presence of normal blood sugar levels, and the natural breakdown of glucose is controlled by insulin. Variables that regulate cellular respiration, including NAD-related substrates, oxygen, succinate, and antioxidant enzymes, modulate ROS levels and sustain cellular redox equilibrium. The conversion of superoxide anions into hydrogen peroxide, before subsequently metabolized into water by catalase and glutathione (GSH) peroxidase, is facilitated by the metalloprotein superoxide dismutase (SOD). Increased ROS levels can lead to diabetic complications, one of which is diabetic retinopathy. Melon superoxide dismutase (SOD) combined with gliadin (Glisodin{\textregistered}) is a potent antioxidant in counteracting free radicals that can reduce oxidative stress and prevent further cell death. Research related to the use of Glisodin{\textregistered} shows potential as an antioxidant agent with the hope of preventing diabetic complications.

}, keywords = {Blood Plasma, Diabetes mellitus, Glisodin{\textregistered}, GSH, SOD, Vitreoretina}, doi = {10.5530/pj.2024.16.197}, author = {Octarina Ervianti and Wimbo Sasono and Reni Prastyani} } @article {2077, title = {Expressions of Matrix Metalloproteinase-3 and Tissue Inhibitor Metalloproteinase-1 in Corneal Tissue Post Alkali Burn Treated with Topical Medroxyprogesterone Acetate and Doxycycline}, journal = {Pharmacognosy Journal}, volume = {15}, year = {2023}, month = {August 2023}, pages = {553-557}, type = {Original Article }, chapter = {553}, abstract = {

Purpose: This study aims to investigate the effects of topical Medroxyprogesterone acetate (MPA) and Doxycycline in inhibiting the expression of MMP-3 and TIMP-1 in ocular alkali burn models in animals. Methods: A total of 18 New Zealand Rabbits were divided into 3 groups based on their post-alkali-burn treatment: PBS (G1/ control group), topical Doxycycline 1mg/ml (G2), and topical MPA 1\% (G3). Alkali burn models were made by exposing 1N NaOH solution to the central cornea for 30 seconds. MMP-3 and TIMP-1 expression were evaluated using immunohistochemistry after 14 days of treatment. Results: Statistically significant differences in the mean MMP-3 expression were found between the three groups (p=0.010). There was a significant difference in MMP-3 expression between the control group with MPA (p=0.017) and Doxycycline (p=0.028) but was not found between the MPA and Doxycycline groups (p=1,000). The mean differences in TIMP-1 expression between the three treatment groups were statistically significant (p=0.005), with a significant difference between the control group with Doxycycline (p=0.022) and MPA (p=0.007). There was no significant difference in TIMP-1 expression between the Doxycycline and MPA groups (P=1,000). Conclusion: This study indicated that topical administration of Doxycycline or MPA in ocular alkali burn reduces the expression of MMP-3 and TIMP-1.

}, keywords = {Corneal alkali burn, Doxycycline., Medroxyprogesterone acetate}, doi = {10.5530/pj.2023.15.118}, author = {Daya Banyu Bening and Reni Prastyani and Nurwasis and Evelyn Komaratih and Ismi Zuhria and Hari Basuki Notobroto and Dyah Fauziah and Chrismawan Ardianto} }