International Journal of Nutrition, Pharmacology, Neurological Diseases

: 2018  |  Volume : 8  |  Issue : 2  |  Page : 41--46

Morin Inhibiting Photocarcinogenesis by Targeting Ultraviolet-B-Induced Oxidative Stress and Inflammatory Cytokines Expression in Swiss Albino Mice

Anjugam Chandrakesan1, Sridevi Muruhan2, Rajeswari Ranga Anantha Sayanam1,  
1 Department of Biochemistry, Vinayaka Mission’s Kirupananda Variyar Medical College and Hospitals, Salem, Tamil Nadu, India
2 Department of Biotechnology, Vinayaka Mission’s Kirupanada Variyar Engineering College, Vinayaka Mission’s Research Foundation (Deemed to be University) Salem, Tamil Nadu, India

Correspondence Address:
Sridevi Muruhan
Vinayaka Mission’s Kirupanada Variyar Engineering College, Vinayaka Mission’s Research Foundation (Deemed to be University), Periyaseeragapadi – 636 301, Salem, Tamil Nadu


Aim: To evaluate the effect of morin in ultraviolet-B (UV-B)-induced oxidative stress and inflammatory cytokines expression in the skin of Swiss albino mice. Materials and Methods: Swiss albino mice were divided into six treatment groups, and each group consisted of eight mice based on their exposure to UV-B radiation (180 mJ/cm2) and their respective treatment with morin (15 mg/kg). Morin was administered both intraperitoneally and topically thrice in a week for 30 weeks before UV-B exposure. After the treatment period, the mice were sacrificed, and the effect of morin on UV-B radiation-induced lipid peroxidation and enzymatic and nonenzymatic antioxidant levels was estimated on skin tissues spectrophotometrically. Western blot analysis was used to estimate the inflammatory cytokines. Results: This study revealed that the intraperitoneal and topical administration of morin significantly lowered the incidence of UV-B-induced tumor size in the skin of Swiss albino mice. Further, morin significantly reduced (P < 0.05) lipid peroxidation and increased the antioxidant levels in Swiss albino mice. It was also observed that morin reduced the expression of tumor necrosis factor-α and interleukin-6. Conclusion: Morin has a stimulative effect on endogenous antioxidant defense mechanisms. It can prevent the photo damage of macromolecules such as lipids and the oxidation of proteins, thereby reducing oxidative stress and inflammation.

How to cite this article:
Chandrakesan A, Muruhan S, Sayanam RR. Morin Inhibiting Photocarcinogenesis by Targeting Ultraviolet-B-Induced Oxidative Stress and Inflammatory Cytokines Expression in Swiss Albino Mice.Int J Nutr Pharmacol Neurol Dis 2018;8:41-46

How to cite this URL:
Chandrakesan A, Muruhan S, Sayanam RR. Morin Inhibiting Photocarcinogenesis by Targeting Ultraviolet-B-Induced Oxidative Stress and Inflammatory Cytokines Expression in Swiss Albino Mice. Int J Nutr Pharmacol Neurol Dis [serial online] 2018 [cited 2022 Jul 1 ];8:41-46
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Clinical and epidemiological studies designate that ultraviolet (UV) radiation, mainly ultraviolet-B (UV-B) (290–320 nm), promotes the development of photocarcinogenesis.[1] Solar UV radiation exerts many effects on the skin including oxidative stress, inflammatory responses, and cell signaling pathway alterations, which lead to the development of skin cancer.[2] The skin possesses antioxidant substances to deal with oxidative stress. UV-B radiation exposure devastates the cutaneous antioxidants and leads to oxidative damage.[3] Dramatic rise in the lipid peroxidation products such as thiobarbituric acid (TBARS) and lipid hydroperoxides (LPH) occurs during chronic UV-B exposure.[4] The important targets of UV-B-induced reactive oxygen species (ROS) are stratum corneum lipids, yielding reactive squalene peroxides as byproducts[5] and hydroperoxy cholesterol species that may play a function in photocarcinogenesis and photosensitivity disorders.[6] Inflammatory responses that activated gene expression and cell proliferation were evoked by increased membrane lipid peroxidation.[7]

Enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and nonenzymatic antioxidants such as glutathione (GSH) and vitamins E and C work synergistically and neutralize the radiation-induced ROS.[8] However, exposure to excessive amounts of UV-B light overcomes these antioxidant defense mechanisms and depletes cellular antioxidant status. The disproportion among the oxidants and antioxidants shifts the cellular redox-sensitive pathways. There are a number of evidences showing the decreased enzymatic antioxidant activities during UV-B exposure.[9]

In the skin, there is a conventional link between tissue damage, inflammation, and cancer development. A chronic inflammation of the skin resulted in the long-term production and accumulation of inflammatory factors associated with tumor development and progression.[10] Inflammatory response triggers a series of events that lead to the transmigration of leukocytes to the injured site. Activated leukocytes cause an abundant production of ROS leading to peroxidative impairment of the skin membranes and contributing to the exacerbation of lesions. Furthermore, these immune cells release growth factors, chemokines, and proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and IL-17, which interact as a network in the pathogenesis of various skin diseases.[11]

Treatment for skin cancer is tedious and causes various side effects. Therefore, preventive steps are necessary. Nowadays, herbal medicines are receiving much importance because of their effectiveness and negligible side effects. A variety of flavonoids and polyphenols derived from the plant have been reported to show antioxidant, anti-inflammatory, antimicrobial, antidiabetic, and anticancer effects.[12],[13],[14] Morin is a bioflavonoid largely isolated from the members of the Moraceae family. Morin present in several fruits and vegetables like osage orange, old fustic, guava leaves, apple, onion and in several beverages such as red wine, tea.[15] Morin exhibits several pharmacological properties such as anticancer, anti-inflammatory, and antioxidant.[16],[17],[18],[19] It has been proven that morin possess very strong inhibitory effect on lipid peroxidation in mouse liver homogenate.[20] It also showed a possible chemopreventive property against some cancers.[21] However, there are no studies on the role of morin in UV-B-induced antioxidant, lipid peroxidation, and inflammatory cytokines activities in an animal model. This study was undertaken to evaluate the same.

 Materials and Methods


The in-vivo experiments were conducted using male Swiss albino mice as an experimental model. The experiments were approved by (Ethical Clearance No. 244) the institutional animal ethical committee of K.M. College of Pharmacy, Madurai, Tamil Nadu, India (certified by CPCSEA, Reg. No. 161/02/CPCSEA). Normal healthy Swiss albino mouse weighing 17–20 g were chosen for this study. Thereafter, the mice were housed in well-ventilated rooms (temperature 65–85°F and humidity 60–70%) with a 13-h light/dark cycle. The mice were maintained on a standard laboratory diet of food and water during the experimental period.

Chemicals and reagents

Morin hydrate, sodium pyrophosphate buffer, phenazine methyl sulphate, dichromate acetic acid, sodium azide, two-dipyridyl solution, GSH reductase, hydrogen peroxide (H2O2), reduced nicotinamide adenine dinucleotide, reduced nicotinamide adenine dinucleotide phosphate, nitro blue tetrazolium, reduced GSH, 2-thiobarbituric acid, and citric acid were purchased from Sigma Chemical Company (St. Louis, MO, USA). All other reagents used were of analytical grade.

Preparation of morin and mode of administration

Morin (15 mg/kg body weight) was dissolved in 0.5% of dimethyl sulfoxide (DMSO) and administered intraperitoneally and topically at a volume of 0.2 ml/kg body weight.

Photocarcinogenesis protocol

Swiss albino mice were categorized into six treatment groups. Each group consisted of eight mice. The mice in Group 1 served as vehicle controls and were given 0.5% DMSO. The animals in Groups 2 and 5 were treated with morin (15 mg/kg body weight) intraperitoneally for 14 days. The animals in Groups 3 and 6 were treated with morin topically (abdomen and dorsal skin) for 14 days. After an interval of 14–31 days, morin treatment was given again thrice a week. Animals in Group 4 were not exposed to UV-B radiation for the first 14 days. Animals belonging to Groups 4–6 were exposed to UV-B irradiation (180 mJ/cm2/day) daily from the 15th to the 24th day. For Groups 5 and 6, morin treatment was performed 1 h before the exposure to UV-B irradiation. The mice were again UV-B irradiated (180 mJ/cm2) thrice in a week after a break of 25–31 days until the end of the experiments.

Ultraviolet-B exposure procedure and evaluation of tumor growth for Swiss albino mice

The skin in the dorsal portions of the Swiss albino mice was shaved using an electric clipper (Oster A2) minimum 2 days prior to the treatment with hair removing cream. The cream was cleaned with warm water and dipped in cotton sorbs. The mice to be used for the experiment were confirmed by ensuring that their skin had no signs of hair regrowth. The dorsal skin was exposed to UV-B radiation with a philips TL40W/12 RS lamp emitting 312 . The UV-B lamp was mounted 20 cm above the table where the mice were placed on. The photocarcinogenesis treatment procedure was performed thrice a week for 30 weeks (UV-B dose was 180 mJ/cm2). The appearance and development of tumors were checked weekly up to the end of the experiment.[22] Growths that were >1 mm in diameter and that persisted for at least 2 weeks were defined as tumors and recorded.

Skin tissue homogenization protocol

The mice were sacrificed by decapitation, and the dorsal skins were removed under anesthesia at various time points. Subcutaneous fat was removed, and the skins were stored at −80°C before use. Whole cell lysates were prepared in a radioimmunoprecipitation assay lysis buffer (120 mM NaCl, 40 mM Tris pH 8.0, 0.1% NP40) containing 1% β-mercaptoethanol, 0.1 M Na3VO4, 0.5 M NaF, and protease inhibitor cocktail and then centrifuged at 13,000×g for 15 min. Supernatants were collected, and they were used as total cell lysates.[23]

Estimation of lipid peroxidation and antioxidant status

The levels of TBARS in the skin tissue were assayed by the methods of Niehaus and Samuelsson.[24] The LPH were evaluated by the method of Jiang et al.[25] The activities of enzymatic antioxidants such as SOD, CAT, and GPx were assayed in the skin tissues by the method of Kakkar et al.; Sinha; and Rotruck et al., respectively.[26],[27],[28] The levels of nonenzymatic antioxidants such as GSH, vitamin C, and vitamin E were estimated on the skin tissues by the method of Ellman; Roe and Kuether; and Baker et al., respectively.[29],[30],[31]

Western blot analysis

An immunoblot (Western blot) analysis by the method of Towbin et al. was performed for TNF-α and IL-6 protein expressions in the skin tissue of mice treated with morin and UV-B irradiation.[32] The results were normalized to β-actin gene expression. Then the samples were subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis for the estimation of protein and were blotted on polyvinylidene fluoride (PVDF) membrane. The primary antibody was added to that and allowed to bind to the protein. Then, the PVDF membranes were washed with Tris-buffered saline with Tween 20 thrice with 10 min interval, and the protein expressions were detected by chemiluminescence substrate (LI-COR, USA). The images were attained by Image Studio software (LI-COR, USA).

Statistical analysis

All the values were expressed as means of six (n = 6) determination. The data were statistically analyzed by the one-way analysis of variance method using the Statistical Package for the Social Sciences (SPSS) (SPSS Inc., Chicago, IL, United States) statistical software, and the group means were compared to Duncan’s multiple range test (DMRT). If the P value was <0.05, it was considered as statistically significant.


Effect of morin on lipid peroxidation products

[Figure 1] shows the effect of morin on TBARS and LPH levels in morin-treated and UV-B-exposed Swiss albino mice. UV-B-exposed animals showed elevated level of TBARS and LPH in the mice skin homogenate. The intraperitoneal and topical application of morin prior to each UV-B exposure resulted in significant reduction of TBARS and LPH levels.{Figure 1}

Preventive effect of morin on enzymatic antioxidant depletion

The data in this study demonstrated that UV-B irradiation resulted in a significant depletion of SOD, CAT, and GPx activities in the mice skin homogenate [Figure 2]. Intraperitoneal and topical treatment with morin significantly prevented the UV-B-induced depletion of enzymatic antioxidant activities and brought back the situation toward normalcy.{Figure 2}

Preventive effect of morin on nonenzymatic antioxidant depletion

UV-B irradiation resulted in the reduction of intracellular GSH, vitamin C, and vitamin E levels in the mice skin homogenate [Figure 3]. Both, the intraperitoneal and topical application of morin, significantly restored the UV-B irradiation-induced depletion of nonenzymatic antioxidant levels.{Figure 3}

Preventive effect of morin on inflammatory cytokines tumor necrosis factor-α and interleukin-6 expression in the skin of ultraviolet-B-induced tumor-bearing mice

UV-B-exposure resulted in the induction of inflammatory cytokine TNF-α and IL-6 in the skin of Swiss albino mice [Figure 4]. The immunoblots revealed that UV-B exposure increased the expression of IL-6 and TNF-α in the skin tissue of mice when compared to the nonirradiated skin of mice. Morin application 1 h before UV-B exposure decreased the expressions of IL-6 and TNF-α proteins when compared to the UV-B-irradiated skin of mice.{Figure 4}


UV radiation, specifically UV-B (280–320 nm) promotes skin cancer development by mutagenic, immunosuppressive, and oxidative stress inducing mechanisms; however, certain antioxidants may neutralize and prevent UV-B-induced photodamage.[33] Polyphenols and flavonoids are widely spread in plants. The flavonoids constitute a large group of compounds containing a number of phenolic hydroxyl groups attached to ring structures, and it possesses significant antioxidant activity.[34] A polyphenol, morin is known to be used as an antioxidant; it acts as a broad-spectrum antibiotic and is also nontoxic.[35]

Oxidative stress plays an important role in UV-B-induced skin carcinogenesis.[36] ROS play a main role in the UV-B-induced depletion of antioxidants.[37] UV-B radiation-induced ROS react with unsaturated fatty acids, proteins, and deoxyribo nucleic acid (DNA) that could result in the breakdown of lipid peroxides, protein–protein cross-links, and DNA strand, all of which can start radical chain reactions and finally enhance oxidative damage.[38] An increased level of lipid peroxidation products including TBARS and LPH in the UV-B-irradiated tumor-bearing skin is probably leads to overproduction of ROS. The intraperitoneal and topical application of morin diminished the lipid peroxidation status in UV-B-exposed skin tissues. This reduction may be due to the free radical scavenging property of the morin, which acts as an antilipoperoxidative agent.[39]

The epidermis layer of the skin contains antioxidant defenses including the enzymes SOD, CAT, and GPx, which remove ROS from the skin. Free radical scavengers such as vitamins C and E, carotenoids, and GSH are also present in the skin to reduce the damaging effects of ROS.[40] The most important mechanism played by SOD is that it helps in transforming ROS and nitrogen species into stable compounds, thereby protecting cells from UV-B damage.[41] CAT and GPx catalyses the conversion of H2O2 into H2O and molecular O2, thus decreasing the damaging effects of H2O2.[42],[43] The intraperitoneal and topical application of morin showed good improvement in the antioxidants status of UV-B-exposed skin tissues. Morin has been proven for its efficient protection of the skin against UVR exposure by elevating the endogenous CAT activity.[44]

UV-B radiation-generated ROS directly causes the depletion of the cellular antioxidant defense system. The intraperitoneal and topical application of morin completely restored the UV-B irradiation-induced depletion of nonenzymatic antioxidants such as GSH, vitamin E, and vitamin C. An earlier study reported that ferulic acid, a phenol, protects the skin form solar-stimulated sunburn cell formation and erythema when given along with α-tocopherol and ascorbic acid.[45] Another study showed that the topical application of sesamol, a polyphenolic compound, completely prevented the UV-B irradiation-induced depletion of GSH, vitamin E, and vitamin C levels,[46] which supports our present work.

Lee et al. examined the protective ability of morin in UV-B-irradiated human keratinocyte stem cells, thereby proving that morin attenuates the secretion of cytokines TNF-α and IL-6.[47] Another study revealed that ferulic acid possessed anticarcinogenic property. It acts against UV-B-induced epidermic tumor development by blocking the relevant cytokine secretion (TNF-α and IL-6) on human keratinocyte cells (HaCaT cells).[48] Thus, from this study, it can be acknowledged that morin decreases the expression of TNF-α and IL-6 in UV-B-irradiated skin of mice.


We suggest that morin seizes photochemopreventive activity through the stimulation of endogenous antioxidant defense mechanisms and the prevention of photodamage to macromolecules such as lipids and the oxidation of proteins. This leads to the reduction in oxidative stress and provides protection against the depletion of the endogenous antioxidant system. The parameters of in-vivo anticancer evaluation and gene expression inhibition showed an enhanced anticancer potential of morin.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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