Subsequently, collagen fibrils were stabilized by intermolecular and intramolecular cross-links with hyaluronic acid (HA). In general, HA attracts water and inflates the gel. HA should compromise the chondroit sulfate (CS) and heparan sulfate (HS), the important components of ECM [1]. HA is a major component of ECM in the vitreous. In the previous study, we postulated that the glycosidic bonds of polysaccharides should be cut and thus, the symptomatic vitreous opacity (SVO) may disappear [2]. According to the past analysis, vitreous liquefaction, flecks of protein, vitreous debris, inflammatory balls, blood particles and torn retina contributed to the SVOs. If left untreated, they could cause impairment of vision and permanent visual loss in the late stage [3]. In general, HA should survive in the intercellular ground and control the function of permeation. Therefore, HA maintains the biodegradable and biocompatible activities [4]. It was found that when vitreouslys happened, the disordered HA could be cut and split, with the shadows on the retina revealing floaters or becoming SVOs [5]. Many patients experienced floaters initially, but generally the symptoms were not troublesome for daily life. Clinics found that SVOs could be associated with floaters, intraocular blood clots and overgrowth of ECM. Patients with more than 10 SVOs or a cloud in front of vision had a high risk of developing retinal tears. The shadow of SVOs on the retina was determined by the diameter of the vitreous opacity, its distance from the retina and the overall distance between the pupillary plane and the retina. If SVOs were removed and absorbed by any method, the ocular floaters would diminish or disappear [6]. Usually the condition is benign and a temporary phenomenon. When SVOs aggregate to fuse together, they may be fixed or mobile especially after the development of posterior vitreous detachment (PVD) [7]. In SVOs, larger members of cobwebs-like shapes may indicate the occurrence of a serious condition such as vitreous hemorrhage (VH) from diabetic retinopathy or trauma. Moreover, ocular dark floaters alone or combined with flashes of light may be the precursor to retinal detachment (RD) or VH [8]. The relationship between floaters and PVD is very close [9]. PVD is a natural change that occurs during adulthood. Several researchers focused on the etiologies of PVD associated with risk factors including age, oxidation and increased proteolytic activity [10]. The incidence of SVO is estimated as 3.1/100,000 per year and the peak incidence occurs between 45 and 65 years old of age [11]. There are various methods for treating SVOs including observation, neodymium-YAG (Nd-YAG) laser and pars plana vitrectomy (PPV). First, observation is the first and most reasonable choice for clinical treatment of ocular floaters. However, the functional effectiveness varies, and the prognosis is beyond the doctor's control [12]. Moreover, PPV was approved as the effective approach in completely clearing the SVOs within the visual axis. The subjects who experienced persistent or severe SVOs may be scheduled to undergo PPV. Equally, vitrectomy for VMT has many disadvantages, with only one-third of eyes gaining two or more lines by Snellen chart [13]. Sometimes, PPV was associated with the patients' economic burden and various postoperative complications such as endophthalmitis and glaucoma [14]. Moreover, RD would occur in 2.4% and 92% of eyes developed into cataract within three years after vitrectomy [15]. Comparing the severe side effects from various treatments leads, many patients to hesitate the invasive approach. Therefore, our purpose is to determine how to develop new, effective and safe methods for treating SVOs. In this study, we designed a capsule containing a mixture of fruit enzymes including bromelain, papain and ficin with the ability to hydrolyze the components of SVOs and cleave the combination of collagen fibrils and HA. In our past study, we demonstrated that consumption of pineapple would decrease ocular floaters.