Liposomal drug delivery for glaucoma: Recent advancement in ocular therapy


Anannya Bose1*, Subhabrota Majumdar2, AsimHalder3

1Department of Pharmaceutical Technology, JIS University, Kolkata -700109, West Bengal, India.

2Calcutta Institute of Pharmaceutical Technology & A.H.S, Uluberia, Howrah -711316, West Bengal, India.

3School of Pharmaceutical Technology, Adamas University, Kolkata -700126, India.

*Corresponding Author E-mail:



Glaucoma affects millions worldwide. Untreated, it might cause lifelong blindness. Traditional treatments have been limited and intrusive. Liposomes are changing glaucoma treatment. Phospholipid bilayer liposomes can carry medications for targeted administration. This innovative glaucoma medication has huge potential to transform the way we treat it. This essay will explain liposomes, how they function, and why they are a glaucoma therapy game-changer. Eyes have several sensory compartments. Eyes send brain impulses. Eye-aqueous humour production causes glaucoma. It mostly affects the over-50s. Glaucoma destroys retinal ganglion cells and the optic nerve, causing blindness. CO2 inhibitors treat it. This inhibitor keeps aqueous humour from the ocular fluid. Normal eye medication dosage. This ocular drug administration approach relies on nasolacrimal drainage and tears turnover to provide the usual dose form. Low bioavailability. Novel pharmaceutical delivery dose formulations can fix this. Nano co-adhesive compositions prolong ocular drug delivery. Liposomes cure glaucoma uniquely. Bioavailability lowers toxicity and dosage. Novel Drug Delivery System helps glaucoma patients worldwide. Liposomes drop IOP slowly. Aqueous liposomes have natural and synthetic phospholipid bilayers. Liposomes contain hydrophilic medicines. Liposomes resemble cells. Their properties make them cling to cells. Biocompatible liposomes increase drug solubility, stability, absorption, and toxicity. Conjunctiva and cornea interactions with liposomes impact tear dynamics and medication duration and frequency. Novel eye medication delivery methods are being investigated. This medicine administration at the proper place challenges drug delivery systems. Here are innovative ocular drug-delivery methods. Biocompatible liposomes improve drug solubility, stability, absorption, and toxicity. Liposomes affect tear dynamics and medication duration and frequency via interacting with the conjunctiva and cornea. Novel ocular medicine delivery techniques for various eye ailments are being explored. This medication administration at the right place challenges drug delivery systems. Innovative ocular drug-delivery systems will be reviewed here.


KEYWORDS: Eye, Ocular barriers, Glaucoma, Liposome, Ocular drug delivery system.




Before designing an eye drug delivery component, you must understand visual life structures and physiology. The eyes are sensitive but crucial organs that indicate causes and tests for medicine delivery. The eyes have many structures like two strong eyebrow curves covering the eyes and including dense hairs that prevent sweating1. Upper and lower eyelids cover the eyes.

The lower eyelid is smaller and less portable than the upper one. Short eyelash hairs1. The lacrimal layer is comprised of the lacrimal organ, which is situated in the sidelong finish of the upper eyelid, and the lacrimal conduit, notwithstanding the lacrimal duct, lacrimal sac, and nasolacrimal organ.


The front portion of the eye has a spherical structure called the eyeball. It includes the outer fibrous layer that forms the sclera. Protects internal organisation and eyeball appearance. The coating forms the cornea. It receives information from sensory nerves3. The middle vascular coat includes the ciliary body, iris, and choroid. Thin, pigmented choroid vascular membrane. The eye's ciliary body is between the iris and choroid. The ciliary muscle exists. The ligament connects to the ciliary muscle. Pigments in the iris membrane affect eye colour.The inner nerve coat Contains the macula. The macula is the eye's innermost nerve layer. It has 8 nerve fibres, nerve cells, a 7 ‘rod’ 6, and ‘cones’ that receive and transmit optic nerve signals. The blind spot is a small area of the macula and the optic disc, a retinal region without either. Direct and near vision are macula-focused4.Light-transmitting structures: Structures that transmit light include: Eye humour is aqueous, lens, and vitreous. Between the anterior and posterior portions is the fluid-watery chamber5.


The lens is hidden behind the iris and the pupil in the human eye. After passing through the pupil, the lens will typically concentrate the light that has reached the retina. The eye's natural shape can be maintained when laughing at violent jokes because of the jelly-like substance of this type of humour. The retina, the choroid, and the sclera are all connected by this toxin-producing humour6.


The anterior and posterior chambers make up the eye. The anterior chamber occupies one-third of the eye and the posterior chamber two-thirds. The anterior part of the eye forms the outside. It faces vitreous humour. The iris includes the cornea, pupil, conjunctiva, ciliary body, lens, aqueous humour, and other eye parts. The posterior part of the eye is hidden by the iris. This governs the eye's inner structure. The sclera, retinal pigment epithelium, choroid, neural retina, and vitreous comprise the posterior section7. To protect the eye from toxicants and be successful in ocular delivery, the drug must overcome substantial difficulties. These ocular obstacles vary with drug delivery. Three types of ocular drug delivery barriers exist: precorneal, static, and dynamic.



Figure 1: The anatomical structure of the eye shows the inside of the eye including the cornea, pupil, lens, ciliary body and muscle, conjunctiva, vitreous body, retinal blood vessels, macula, optic nerve, and retina.


A few disease conditions that can disturb the front of the eye include cataracts, glaucoma, allergic conjunctivitis, and anterior uveitis8. Diseases that are predominantly brought on by ageing affect the posterior portion of the eye. Posterior region problems of the eye are the most common cause of vision loss in the industrialised world. Examples include posterior illnesses such as diabetic eye disorder, age-related macular degeneration (AMD), and another region of the eye. Blood capillaries in the retina and beneath the conjunctiva are absorbed systemically8. The nasolacrimal duct, as well as the outflow from it, reduces medication absorption. It’s a treatment that’s applied to the skin.


Obstacles To Intraocular Drug Transportation:

Tear layer:

Tears are the eye's first chemical barrier. An enzyme-rich aqueous layer blocks lipophilic medications and mucus after lipids inhibit absorbent drugs9. The 0.02-0.05 m broad later clings to all microbes and surfaces due to low harmony polyvalent adhesive reactions. 1L/min tear turnover lowers drug absorption after delivery, enhancing drug clearance and cleaving proteins with impermeable active drug components. The average ocular injection is 20–50 L.



Epithelium, stroma, and endothelium make up the cornea, the eye's main refracting surface. Mechanically blocks external objects from sight. Different barriers block medicines from entering these levels. Strong cellular connections and lipophilic corneal epithelium reduce paracellular drug transfer. Stromal collagen fibrils' hydrated lamellar structure prevents hydrophobic molecules9. The corneal endothelium's hexagonal cells separate stroma and aqueous humour. Macromolecules travel via defective endothelium junctions. The paracellular route may allow medicines to penetrate cells and transcellularly reach the stroma through the epithelium.



The conjunctiva's blood vessels expand and maintain the tear film. Medication is removed quickly through the bloodstream or lymphatic system. Pinocytosis and convective transport via the vascular endothelium layer's paracellular pores allow medicines, especially high-molecular-weight proteins and peptides, to reach the bloodstream through the conjunctival veins' porous barrier. Certain drugs may also penetrate the posterior conjunctiva via transscleral penetration.



Vascularity-wise, the choroid has 10 times more blood flow per unit of tissue weight than the brain. The 20–40-m-wide choroidal capillary endothelium with fenestrations is also distinctive10. Older people have thinner choroidal thickness. Drug penetration into the retina and vitreous may depend on choroid thickness.


Blood–Retinal- barriers:

The BRB and BAB are in the intraocular environment. The BAB's non-pigmented ciliary body epithelium blocks medication molecules from accessing the intraocular environment and organizes active and paracellular transport. BRB blocks bloodstream medication molecules from entering the posterior. The retinal capillary endothelial cells and retinal pigment epithelium cells form the internal and exterior blood-retinal blockades. A monolayer of cells, RPE preferentially transports molecules between photoreceptors and choriocapillaris. It's between the choroid and neuronal retina. RPE tight connections effectively limit intercellular permeability. Due to its high vascularity, medicinal drugs can enter the choroid from the bloodstream, but RPE inhibits them from entering the retina. Thus, systemic rather than topical retinal drug treatment may be superior.



Glaucoma encompasses a variety of diseases with various causes, risk factors, demographics, indications, periods, management, and outcomes. Worldwide, glaucoma causes more irreversible blindness than cataracts.1–3 Pathophysiologically and therapeutically, intraocular pressure is the key vision risk factor. Intraocular pressure lowers 30–50%, stopping glaucoma growth. This link displays glaucoma patients' high intraocular pressure versus optic nerve head pressure vulnerability. Beginning with glaucomatous optic nerve injury. All types of glaucoma involve retinal ganglion cell loss, retinal nerve fibre layer fading, and optic disc cupping. The shape of the angle at the front of the anterior compartment divides glaucoma into open-angle and angle-closure types. Schlemm's canal is located inside the anterior chamber angle between the peripheral cornea and iris. ÜberSchlemm's canal, ocular aqueous humour leaves. Many patients' intraocular pressure, the biggest risk factor for glaucoma, is just slightly higher or within the normal range, and any increase is usually painless. Intraocular pressure is the biggest glaucoma risk. Early diagnosis is necessary to prevent subjective symptoms from chronic glaucoma, which may not be recognized until late in the condition when central visual acuity and reading skills are compromised. This Seminar will discuss glaucoma epidemiology, pathogenesis, symptoms, identification, and management, as well as potential discoveries. Our purpose is to summarize these themes11.



Glaucoma blinded 6.1% of the world's 4 million blind in 2010. 4.2 million (2% of 191 million visually handicapped people) suffer from glaucoma. Vision loss occurs when the better eye has reduced acuity. Youth have lower glaucoma rates than high-revenue countries with older populations. Glaucoma increases with age. Glaucoma affects 3.5% of 40–8019-year-olds worldwide. About 3.1% of persons globally had main open-angle glaucoma and 0.5% primary angle closure. Crucial open-angle glaucoma was six times as common as primary angle closure. Africa (4.2%) had the most primary open-angle glaucoma, while Asia (1.1%) had the most primary angle-closure. Glaucoma affected 64.3 million 40–80-year-olds globally in 2013. This will climb to 76 million in 2020 and 112 million in 2040. Men and Africans had higher rates of primary open-angle glaucoma than women and Europeans (OR 2:80). Primary angle-closure glaucoma had more bilateral blindness than open-angle, suggesting a worse prognosis 12.



Glaucoma is a prevalent trigger of visual loss due to optic neuropathy all around the world. Glaucoma, on the other hand, is rarely linked with visible symptoms until it has progressed to the point where it poses a significant risk to patients.Glaucoma is an ocular sickness. It arises when the fluid pressure in the eye increases to a level that damages the optic nerve, causing the patient to lose vision and perhaps become blind. This form of ocular illness occurs when the intraocular pressure rises owing to an excess of fluid from the aqueous humour in the eye. This condition primarily affects middle-aged and older people. Millions of people suffer from progressive optic neuropathy. Glaucoma is a dangerous neurodegenerative disorder that requires effective treatment13. The development of intraocular pressure is the key factor in this condition. Retinal ganglion cells are injured as a result of this, and the optic nerve is affected, resulting in vision damage. As a result, this is the most prevalent cause of permanent blindness.


Open-angle glaucoma:

Known as chronic sickness. The illness will develop gradually. Eye pressure rises as drainage channels get blocked, causing glaucoma. It features a wide-degree angle between the iris and cornea. This condition is lifelong. Signs and symptoms are ignored. The “open angle” is the iris-cornea junction. Another name for glaucoma is primary or chronic. As the optic nerve degenerated in primary open-angle glaucoma, intraocular pressure climbed. Low-tension or normal-pressure glaucoma damages the optic nerve despite normal eye pressure. In secondary glaucoma, the cause of high eye pressure, which impairs the optic nerve and causes vision loss, can be determined 14.

Angle-closure glaucoma:

This sickness is sudden and painful. Vision loss occurs quickly due to clogged drainage routes, which raise eye pressure unexpectedly. Closed or narrow-angle between iris and cornea. Indications and damage stick out. Patients seek medical help for pain and discomfort to avoid irreparable damage. In primary angle closure glaucoma, the anterior chamber angle narrows and blocks aqueous humour outflow. Secondary angle-closure glaucoma occurs when the angle between the iris, the red component of your eye, and the cornea, the transparent glass in front of it, narrows or shuts due to a known cause of abnormal blood vessel development (neo-vascular glaucoma)15.



Figure 2. Open-angle glaucoma and closed-angle glaucoma. The red arrow shows the direction of the flow of aqueous humour in the anterior chamber of the eye.



In ophthalmology, nanotechnology can be used to diagnose, evaluate, and treat glaucoma. Liposomes are a popular nano vesicular device for ocular medicine administration because they increase contact time and corneal retention. Long-term corneal retention increased topical bioavailability, reduced administration, and improved patient acceptance. Due to their biocompatibility, biodegradability, protection from the environment, and ability to bypass many physiological barriers, liposomes are the best drug carriers for hydrophobic and hydrophilic agents16. Liposomes carry hydrophilic and hydrophobic drugs. They release medicine based on temperature, electromagnetic radiation, and pH. Ophthalmic glaucoma therapies predominate17. In eye drops, fewer than 1% of oral medicine reaches aqueous humour and works. Blinking reflux and tear production result in a rapid ocular outflow of remaining medicine, requiring repeated administration and patient noncompliance. Liposomes can be made using extrusion, French press, reverse phase evaporation, microencapsulation vesicle method, thin film hydration, and ethanol injection. For liposome formulation, lipid compositions, vesicle size, surface charge, and manufacturing method must change.Temperature-sensitive, pH-dependent, ligand-based liposomes distribute medicines. Zero-order kinetics of rapid and persistent drug release are shown in several investigations. Medication discharge control may improve targeting18. Time can damage shell width, material, and particle size.  Drug retention depends on liposome charge. Positively charged liposomes adhere, remain longer, penetrate, and entrap better because the cornea's mucinous barrier renders the epithelial surface negatively charged. Several pharmaceutical distribution technologies have been studied to solve conventional dose form issues throughout the past decade. Liposomes, dendrimers, nanoparticles, and niosomes reduce side effects and improve medication absorption19. Over a decade, liposomal drug delivery formulations have been studied. The last 40 years have seen enormous developments in liposome research. For diverse purposes, liposomes might vary in size, phospholipid, cholesterol, and surface morphology. Liposomes bind cells differently. Liposomes, a better carrier, have been examined for ocular medicine delivery. Flexible liposomes have been widely explored for front and posterior eye disorders. Bioadhesive and penetration-enhancing polymers improve corneal adherence and medication permeability in anterior routes. Improve even posterior section deformities.


To improve corneal adhesion and permeation, bioadhesive and penetration-enhancing polymers are used to deliver anterior segment drugs. In posterior portion dysfunction, intra-vitreal half-life and retinal medication delivery must be improved. Subfoveal choroidal neovascularization (CNV), ocular histoplasmosis, and pathological myopia are treated with verteporfin photodynamic therapy. The light activates the bloodstream drug verteporfin. After the drug is administered, a low-energy laser activates verteporfin in the retina through the contact lens, collapsing abnormal blood vessels.



Figure 3: Schematic representation of the liposome. Liposomes consist of a lipid bilayer that can be composed of cationic, anionic, or neutral (phospho)lipids and cholesterol, which enclose an aqueous core. Both the lipid bilayer and the aqueous space can incorporate hydrophobic or hydrophilic compounds, respectively.


Liposomes have a prolonged effect on intraocular pressure reduction. Liposome particles, such as (SUV), are small enough to cause less abrasion, irritation, and sensitivity, yet they’re powerful enough to link with tissues and transport drugs more effectively. Liposomes are a kind of ocular delivery system that has the potential to increase retention duration while lowering intraocular pressure. Traditional dose forms, such as solutions and suspensions, have issues with limited absorption, nasolacrimal drainage, tear turnover, and drug loss on the eyelids. Contrarily, liposomes enhance the drug’s extended or controlled release, which boosts bioavailability. The effectiveness of therapeutic therapies has therefore managed to increase. The prolonged drug release possessions of timolol maleate gelatinized core liposomes make them a unique, reliable, and stable glaucoma treatment. Vesicles were created using the thin-film hydration method and then examined for stability and drug release in vitro. In vivo, testing was done to see if reducing intraocular pressure (IOP) might help glaucomatous rabbit eyes. Examinations of the histopathology were utilised to assess the safety profile20.The particle size, 38.81 m, Gelatin meaning fully augmented drug encapsulation percentage, reaching 50%, with a particle size of 38.81 m. The resulting vesicles produced the most benign histological findings and the greatest reduction in IOP. The main difficulties with ophthalmic liposomal preparations of hydrophilic drugs were addressed by this research, leading to the creation of timolol maleate gelatinized core liposomes, a novel, safe, and efficient ocular glaucoma therapy21.Monem et al. examined the consequence of liposome surface charge on IOP decrease in rabbits. Neutral liposomes containing pilocarpine reduced IOP in rabbits’ eyes in a manner similar to that of traditional ocular drops or negatively charged liposomes, nonetheless, it remained two times extended, prolonging drug residential duration by ten hours, and lowering IOP. Using neutral liposomes, the IOP was dropped from 20.7 mmHg to 15 mmHg after 30 minutes, and the lower IOP persisted for 4-5 hours. Negatively charged liposomes exhibited a nearly one-third shorter pharmacological impact than neutral liposomes22.Egg-phosphatidylcholine liposomes measuring 18 nm were administered.  When compared to topical latanoprost, subconjunctivallatanoprost improved stability and decreased IOP for up to 90 days (4.8 1.5 mmHg) in rabbit eyes The disadvantage of liposomes should be their propensity for aggregation, which might result in issues like drug leakage.  They are similarly susceptible to phagocytosis, but this is prevented by surface modification, which has helped with the treatment of these complications. Bioadhesive polymers that are coated on liposomes prevent aggregation and encourage viscosity. Six recipients of the injection who had ophthalmic hypertension or primary open-angle glaucoma did well tolerating it. IOP was 27.55 3.25 mmHg at baseline, and it decreased by a mean of 13.03 2.88 mmHg, or 47.43 10.05 per cent, on average. IOP decreased after three months in a clinically and statistically meaningful manner (20%, p 0.05). Although it’s also likely that the bound medication was not removed from the eye fast, retaining of latanoprost inside the anterior compartment and ongoing drug release from the liposomal formulations both contributed to the persistent IOP-lowering effect. To extend the ocular levels of 5-FU during glaucoma filtration surgery, Simmons et al. created a liposomal delivery method. They discovered that liposomal 5-FU increased the amounts in the sclera and conjunctiva, lowering the peak ocular concentrations in the process. Liposomal 5-FU may therefore assist in lessening the possibility of adverse ocular effects while also improving the surgical success of glaucoma surgery23. A cancer-fighting anthracycline medication called daunorubicin stops the synthesis of DNA. In glaucoma filtration surgery, daunorubicin was demonstrated by Varma et al. to be both safe and effective at lowering intraocular pressure.A rabbit model of proliferative vitreoretinopathy was used by Shinohara et al. to demonstrate the effectiveness of daunorubicin encapsulated in empty liposomes. When using liposomal daunorubicin, the researchers did not note any negative adverse effects.



For glaucoma diseases, liposomes provide a medication that can be administered for a prolonged period. By increasing the corneal contact duration, this formulation enhances the drug’s ocular bioavailability. Drainage, lacrimation, and conjunctival absorption are all avoided by these liposomes. As a result, it’s very effective in the treatment of glaucoma. This formulation provides functional recovery and greater compliance, and it is used to enhance the therapeutic effects of glaucoma drugs. Liposomes are simple to use and can be delivered by the patient himself. They potentially reduce the toxicity of a drug’s administration24.



This glaucoma treatment liposome formulation causes visual impairment. It’s difficult to find and remove them from the eye. When you sleep or touch your eyes, liposomes are lost. The pharmacological properties of drugs and the different lipid types used to formulate liposomes influence where drugs are included. Liposomes have a numeral of advantages as a carrier for ophthalmic drug delivery. They’re convenient to use and can maintain therapeutic efficacy at the appropriate spot for a long time. Patient compliance is high as a result of this. Liposomes have subconjunctively given latanoprost-loaded liposomes with a diameter of 103.18 5.1 nm. A long-lasting influence on the cornea’s surface and control drug absorption. They prevent drugs from being broken down by enzymes existing in tears and on the epithelial surface of the cornea. Liposomes assist in overcoming the disadvantages of repeated use because of this property25.



Topically drug-centred techniques and surgical-centred methods are together used to treat glaucoma. Both strategies are aimed at preventing vision loss, slowing disease progression, and preserving well-being. Improving uveoscleral outflow and traditional trabecular outflow, as well as decreasing aqueous humour generation, are now the most frequent methods for lowering intraocular pressure. Drug-based methods are often used to recover from open-angle glaucoma in the early stages, but surgery may be required in more advanced instances. In congenital glaucoma, surgery is also a choice. Whereas in pigmentary glaucoma and angle closure glaucoma, laser treatment is a common choice.


Most drugs in conventional dosage forms are wasted due to nasolacrimal drainage and tear turnover in the drug delivery pathway to the eye. As a result, their bioavailability becomes low. Using novel drug delivery dosage forms, this problem can be addressed, and the deficiencies in the mechanism for administering the medication into the eye can be avoided. Nanoparticulate, small vesicle-like liposomes, and Nano cohesive formulations are all potential aspects to improve glaucoma treatments.


The novel medication delivery system provides prolonged or controlled drug delivery by introducing the medicine into the cull de sac cavity. The approach for providing controlled provides a variety of advantages over normal dosage forms, including enhanced drug bioavailability, decreased toxicity, and lower dose frequency. Patients with glaucoma are open to new drug administration methods. Novel medication distribution methods for glaucoma therapy are now generally recognized by glaucoma patients due to their multiple benefits.



Nanoscience and nanotechnology have recently played a crucial part in the growth of novel ocular disorder treatments. To connect to Nanocarriers, a variety of active chemicals have been developed. This is used to quickly engage with specific eye tissues and break down ocular barriers. A range of eye illnesses, including corneal disease, glaucoma, retina disease, and choroid disease, may now be treated with nanotechnology-based remedies. The present treatment technique very seldom completely recovers vision loss or discovers serious eye illness early on. By aiding with bioadhesive enhancement, long-term release, precisely targeted dispersion, and stimuli-sensitive release, nanotechnology is revolutionizing eye disease care.



The goal of the nanosystem for ocular disease treatment is to produce drug delivery to both the front and back of the eye. Both traditional and alternative approaches can be applied, according to current nanotechnology research. The topical method of medication delivery is highly effective for glaucoma therapy. Taking a systematic approach is more important than administering drugs. The corneal route allows drugs to penetrate the eye’s interior tissues. To take medications topically, the transcellular and paracellular routes, which are two key corneal trafficking channels, are employed.


In the eye, the corneal epithelial layer acts as a barrier to trans corneal permeability. After hydrophilic pharmaceuticals have passed via the paracellular pathway, lipophilic medications go through the cornea through the transcellular pathway. Drugs such as beta-blockers, cholinergic agonists, carbonic anhydrase inhibitors, and adrenergic agonists are used to treat glaucoma.



Microemulsions, liposomes, dendrimers, nanoparticles, transparent high-viscosity gels, and other technologies for generating and delivering customized corneal permeability drugs enhance their nature. This revolutionary drug delivery technique may help overcome patient compliance issues and give local, long-lasting treatment with minimal side effects. Beta-blockers and adrenergics also lower choroidal and optic disc blood flow. Anti-glaucoma medications improve vision and treat glaucoma. Innovative drug delivery devices can lower intraocular pressure and prolong retinal ganglion cells. Research on future glaucoma therapeutics will leverage these unique targets25.



Topical glaucoma medicines are key. Novel delivery technologies interact better with tissue and disperse medications more effectively, reducing abrasion, irritation, and sensitivity. An innovative drug delivery system can increase precorneal residence time and drug corneal permeability for targeted anti-gluconate treatment. Poor bioavailability, therapeutic effectiveness, dosage frequency, patient adherence, and compliance can be improved while side effects and deadly consequences are reduced.



The authors have no conflicts of interest regarding this investigation.



The author thanks Prof. Dr. Subhabrota Majumdar, Calcutta Institute of Pharmaceutical Technology & Allied Health Sciences, Uluberia, Howrah and Dr. AsimHalder, School of Pharmaceutical Technology, Adamas University, Kolkata -700126, India, for the critical reading of the manuscript.



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Received on 21.07.2023            Modified on 03.10.2023

Accepted on 20.11.2023           © RJPT All right reserved

Research J. Pharm. and Tech 2024; 17(4):1741-1747.

DOI: 10.52711/0974-360X.2024.00276