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. 2023 Jun 3;12(11):2210.
doi: 10.3390/plants12112210.

Bioefficacy of Nga-Mon (Perilla frutescens) Fresh and Dry Leaf: Assessment of Antioxidant, Antimutagenicity, and Anti-Inflammatory Potential

Payungsak Tantipaiboonwong  1 , Komsak Pintha  1 , Wittaya Chaiwangyen  1 , Maitree Suttajit  1 , Chakkrit Khanaree  2 , Orawan Khantamat  3
Affiliations

Bioefficacy of Nga-Mon (Perilla frutescens) Fresh and Dry Leaf: Assessment of Antioxidant, Antimutagenicity, and Anti-Inflammatory Potential

Payungsak Tantipaiboonwong et al. Plants (Basel). .

Abstract

Perilla leaves are known to be a rich source of polyphenols, which have been shown to exhibit various biological effects. This study aimed to compare the bioefficacies and bioactivities of fresh (PLEf) and dry (PLEd) Thai perilla (Nga-mon) leaf extracts. Phytochemical analysis indicated that both PLEf and PLEd were abundant in rosmarinic acid and bioactive phenolic compounds. PLEd, which had higher levels of rosmarinic acid but lower levels of ferulic acid and luteolin than PLEf, exhibited greater effectiveness in a free radical scavenging assay. Furthermore, both extracts were found to suppress intracellular ROS generation and exhibit antimutagenic activity against food-borne carcinogens in S. typhimurium. They also attenuated lipopolysaccharide-induced inflammation in RAW 264.7 cells by inhibiting the expression of nitric oxide, iNOS, COX-2, TNF-α, IL-1β, and IL-6 through the suppression of NF-κB activation and translocation. However, PLEf exhibited a higher ability to suppress cellular ROS production and higher antimutagenic and anti-inflammatory activities than PLEd, which can be attributed to its combination of phytochemical components. Overall, PLEf and PLEd have the potential to serve as natural bioactive antioxidant, antimutagenic, and anti-inflammatory agents to achieve potential health benefits.

Keywords: Nga-mon; Perilla frutescens; anti-inflammation; antimutagenicity; antioxidant.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Antioxidant capacity of PLEs: (A) the scavenging of DPPH and (B) ABTS radicals. Data represent the mean of three independent triplicate experiments (n = 3). Error bars indicate SD.
Figure 2
Figure 2
The cytotoxic effect of PLEf and PLEd on (A) PBMCs and (B) RAW 264.7 cells at 48 h. Data represent the mean of three independent triplicate experiments (n = 3). Error bars indicate SD.
Figure 3
Figure 3
Intracellular ROS production in PBMCs. Data represent the mean of three independent triplicate experiments (n = 3). Error bars indicate SD. * p < 0.05, *** p < 0.001 versus no extract treatment.
Figure 4
Figure 4
Effect of PLEs on (A) NO production and (B) cell viability of LPS-treated RAW 264.7 cells. Data represent the mean of three independent triplicate experiments (n = 3). Error bars indicate SD. ** p < 0.01, *** p < 0.001 versus LPS without extract treatment.
Figure 5
Figure 5
Effect of PLEs on LPS-induced mRNA expression of (A) iNOS and (B) COX-2 in RAW 264.7 cells. Data represent the mean of three independent triplicate experiments (n = 3). Error bars indicate SD. ** p < 0.01, *** p < 0.001 versus LPS without extract treatment.
Figure 6
Figure 6
Effect of PLEs on LPS-induced iNOS and COX-2 production in RAW 264.7 cells. The cells were pretreated with different concentrations of PLEs for 2 h and then co-treated with 1 µg/mL of LPS for 22 h. iNOS and COX-2 levels in whole-cell lysate were detected through the Western blot analysis, and the data from a typical experiment are presented. Similar results were obtained from two independent experiments (n = 2). Error bars indicate SD. * p < 0.05, *** p < 0.001 versus LPS without extract treatment.
Figure 7
Figure 7
Effect of PLEs on LPS-induced (A) TNF-α and (B) IL-6 production in RAW 264.7 cells. Data represent the mean of three independent triplicate experiments (n = 3). Error bars indicate SD. ** p < 0.01, *** p < 0.001 versus LPS without extract treatment.
Figure 8
Figure 8
Effect of PLEs on LPS-induced (A) TNF-α, (B) IL-6, and (C) IL-1β mRNA expression in RAW 264.7 cells. Data represent the mean of three independent triplicate experiments (n = 3). Error bars indicate SD. * p < 0.05, *** p < 0.001 versus LPS without extract treatment.
Figure 9
Figure 9
Effects of PLEs on LPS-induced (A) NF-κB and (B) AP-1 activation in RAW 264.7 cells. The cells were pretreated with various concentrations of PLEs for 12 h and then co-treated with 1 μg/mL of LPS for 45 min. The total NF-κB p65 and its phosphorylation levels in the whole-cell lysate were detected through Western blot analysis, and the data from a typical experiment are presented, while similar results were obtained from three independent experiments (n = 3). Nuclear extracts were prepared in order to analyze the nuclear translocation of AP-1 (c-Jun), and the data represent the mean of two independent experiments (n = 2). Error bars indicate SD. * p < 0.05, ** p < 0.01 versus LPS without extract treatment.
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