Topical route of administration is the most commonly used method for the treatment of ophthalmic diseases. However, presence of several layers of permeation barriers starting from the tear film till the inner layers of cornea make it difficult to achieve the therapeutic concentrations in the target tissue within the eye. In order to circumvent these barriers and to provide sustained and targeted drug delivery, tremendous advances have been made in developing efficient and safe drug delivery systems. Liposomes due to their unique structure prove to be extremely beneficial drug carriers as they can entrap both the hydrophilic and hydrophobic drugs. The conventional liposomes had several drawbacks particularly their tendency to aggregate, the instability and leakage of entrapped drug and susceptibility to phagocytosis. Due to this reason, for a long time, liposomes as drug delivery systems did not attract much attention of researchers and clinicians. However, over recent years development of new generation liposomes has opened up new approaches for targeted and sustained drug delivery using liposomes and has rejuvenated the interest of researchers in this field. In this review we present a summary of current literature to understand the anatomical and physiological limitation in achieving adequate ocular bioavailability of topically applied drugs and utility of liposomes in overcoming these limitations. The recent developments related to new generation liposomes are discussed.

Glaucoma, the second leading cause of blindness, is characterized by changes in the optic disc and visual field defects. The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons. Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death. A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options. This review is an effort to summarize the current concepts in the pathophysiology of glaucoma so that newer therapeutic targets can be recognized. The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

Purpose. To investigate the anti-inflammatory effect of topical application of Curcuma longa (C. longa) and Berberis aristata (B. aristata) aqueous extracts on experimental uveitis in the rabbit. methods. Anterior uveitis was induced in rabbits by intravitreal injection of lipopolysaccharide from Escherichia coli after pretreatment with C. longa and B. aristata aqueous extracts. Subsequently, the anti-inflammatory activity of C. longa and B. aristata was evaluated by grading the clinical signs and histopathologic changes and estimating the inflammatory cell count, protein, and TNF-α levels in the aqueous humor. results. The anterior segment inflammation in the control group was significantly higher than in both the extract-treated groups, as observed by clinical and histopathologic grading. The inflammatory cell count in the control group was 30.75 ± 7.33 × 10⁵ cells/mL, whereas it was 2.39 ± 0.59 × 10⁵ (P < 0.001 vs. control) and 11.56 ± 2.44 × 10⁵ (P = 0.001 vs. control) cells/mL in the C. longa– and B. aristata–treated groups, respectively. The protein content of the aqueous humor was 18.14 ± 4.98, 3.16 ± 0.55 (P < 0.001 vs. control), and 8.24 ± 1.42 (P < 0.01 vs. control) mg/mL in the control, C. longa–, and B. aristata–treated groups, respectively. The aqueous TNF-α level in the control group was 976.29 ± 66.38 pg/mL and was 311.96 ± 28.50 (P < 0.0001 vs. control) and 654.09 ± 47.66 (P < 0.001vs. control) pg/mL in the C. longa– and B. aristata–treated groups, respectively. conclusions. Topical instillation of aqueous extracts of C. longa and B. aristata showed potent anti-inflammatory activity against endotoxin-induced uveitis in rabbits.

Glaucoma, a neurodegenerative disease, is currently being treated by modulation of one of its primary risk factors, the elevated intraocular pressure. Newer therapies that can provide direct neuroprotection to retinal ganglion cells are being extensively investigated. Tumor necrosis factor-α, a cytokine, has been recognized to play an important role in pro and antiapoptotic cellular events. In this paper we review the relevant literature to understand (1) The association of increased expression of tumor necrosis factor-α with glaucomatous neurodegeneraion, (2) Modulation of tumor necrosis factor-α expression by exposure to various risk factors of glaucoma, (3) Downstream cellular signaling mechanisms following interaction of tumor necrosis factor-α with its receptors and (4) Role of tumor necrosis factor-α as a possible target for therapeutic intervention in glaucoma. Literature was reviewed using PubMed search engine with relevant key words and a total of 82 English language papers published from 1990 to 2010 are included in this review.