Application of an active peptide in the preparation of products for improving mitochondrial function and anti-wrinkle and anti-inflammatory

Abstract

The present invention discloses the application of active peptides in the preparation of products for improving mitochondrial function and anti-wrinkle and anti-inflammatory. The active peptide is an active peptide SA-LFP with an amino acid sequence of CLAGRRRRSV, or a derivative palmitoylated modified SA-LFP active peptide, an acetyl modified SA-LFP active peptide, a cyclized SA-LFP active peptide, or a biotin modified SA-LFP active peptide. The present invention relates to a new application of active peptides in improving mitochondrial function and anti-wrinkle and anti-inflammatory. The active peptides target mitochondria and can achieve anti-wrinkle and anti-inflammatory activity by regulating and improving mitochondrial function, and have high production application value.

Description

Technical Field

[0001] The invention belongs to the field of biotechnology and relates to the application of active polypeptides in the preparation of products for improving mitochondrial function and anti-wrinkle and anti-inflammatory. Background Art

[0002] Mitochondria are very important organelles in cells, with genetic material (mtDNA) independent of the cell nucleus and corresponding gene transcription and protein translation systems. Mitochondria are involved in a variety of metabolic and regulatory functions, including fatty acid and amino acid metabolism, biomolecule synthesis, calcium regulation, antiviral defense and cell signaling. Mitochondria are essential for maintaining the life activities of cells and even the entire organism. They not only provide power for cells, but also can potentially trigger inflammation and cell death. Mitochondrial dysfunction is one of the hallmarks of human aging. The hallmarks of human aging include 5 main hallmarks: genomic instability, telomere attrition, epigenetic changes, loss of protein homeostasis, and macroautophagy failure; 3 antagonistic hallmarks: nutrient sensing disorders, mitochondrial dysfunction, and cell aging; and 4 comprehensive hallmarks: stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis (Hallmarks of aging: An expanding universe). Mitochondrial dysfunction refers to a state in which mitochondria are impaired in terms of energy metabolism, apoptosis, cell cycle control, oxidative stress response, etc., usually accompanied by enhanced ROS production and NAD + decreased mtDNA damage, decreased antioxidant defense mechanisms, altered cellular respiration, altered metabolism, and enhanced cell death.

[0003] Mitochondria, also known as the "energy factory of cells", play a core role in energy metabolism. They produce ATP through the process of oxidative phosphorylation, and the generated ATP can meet the high energy demand of skin cells. They play an important role in maintaining skin homeostasis and skin elasticity. When mitochondrial function is impaired, these functions will be affected. Because mtDNA damage and high ROS can affect ECM synthesis, the secretion of growth factors and cytokines, leading to skin wrinkles, pigmentation and other skin aging characteristics, there are even studies showing that mtDNA damage is the potential root cause of skin aging (Research progress of mitochondria in skin photoaging), so restoring mitochondrial function can remove skin wrinkles and restore skin elasticity. At present, the anti-wrinkle peptides on the market are mainly divided into signal peptides, neurotransmitter inhibitory peptides, carrier peptides and other functional peptides. Among them, palmitoyl tripeptide-5 and palmitoyl pentapeptide-4 are signal peptides, which mainly increase skin thickness and reduce wrinkles by stimulating collagen synthesis. Neurotransmitter inhibitory peptides mainly include acetyl hexapeptide-8 and snake venom peptides. These peptides relax facial muscles by locally blocking nerves to transmit muscle contraction messages to achieve anti-wrinkle purposes. Acetyl hexapeptide-8 can only achieve immediate anti-wrinkle effect, but cannot delay or even reverse the formation of wrinkles from the source. Therefore, the development of anti-wrinkle active peptides targeting mitochondria can fight skin wrinkles from the source and has great application prospects.

[0004] As damage-associated molecular patterns (DAMPs), mtDNA and ROS released from mitochondria can activate NLRP3 inflammasomes, further promoting the secretion of inflammatory factors IL-1β and IL-18. In addition, mitochondrial dysfunction can promote the production of SASP and induce chronic inflammation. SASP includes TNF-ɑ, IL-6, IL-1, IL-8 and MMP. Studies have found that MFN1 can activate the mt-dsRNA / MAVS / SASP axis to regulate SASP. Genetic or pharmacological inhibition of MFN1 can weaken SASP (Release of mitochondrialdsRNA into the cytosol is a key driver of the inflammatory phenotype of senescent cells). There are two main types of anti-inflammatory drugs used today, corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs). These drugs have strong side effects, such as hepatotoxicity, gastrointestinal toxicity and anaphylactoid reactions. Therefore, anti-inflammatory active peptides with high safety have great application prospects.

[0005] Mitochondria are dynamic organelles surrounded by two membranes in eukaryotic cells. They participate in essential energy metabolism, redox signals, and intracellular signal transduction by maintaining mitochondrial dynamic homeostasis. Mitochondrial dynamics refers to the changes in the morphology, number, and position of mitochondria, such as fission, fusion, mitophagy, and transport. Peroxisome proliferator-activated receptor γ coactivator 1ɑ (PGC-1ɑ) affects the transcription of mitochondrial genes and the increase in the number of mitochondria by regulating the activity of a series of nuclear transcription factors, including mitochondrial transcription factor A (TFAM), nuclear respiratory factor 1 (NRF1), and NRF2. It can also promote mitochondrial biogenesis, regulate energy metabolism, enhance the ability to resist oxidative stress, and synergize with the AMPK / SIRT1 signaling pathway. PGC-1ɑ plays a core role in regulating mitochondrial function (PGC-1ɑIs aMaster Regulator of Mitochondrial Lifecycle and ROS Stress Response). MFN1 and MFN2 are located in the outer membrane of mitochondria and mainly regulate the fusion of the outer membrane of mitochondria. The regulation of the inner membrane of mitochondria is mainly through OPA1. SIRTs are involved in multiple biological pathways and are closely related to energy metabolism, oxidative metabolism, etc. They play an important role in neuronal differentiation, genome stability and cell survival. SIRT3 and SIRT4 are longevity genes located in mitochondria and play an important role in mitochondrial homeostasis and metabolic regulation. SIRT3 can deacetylate the ETC complex to promote efficient electron transfer and promote mitochondrial biogenesis, thereby reducing the generation of ROS and maximizing the production of ATP, and enhancing the mitochondrial antioxidant defense system (Epstein Lecture: Sirtuins, aging, and medicine); SIRT4 plays an important role in regulating ATP homeostasis and can enhance the ability of the genome to repair after DNA damage (SIRT4 interacts with OPA1 and regulates mitochondrial quality control and mitophagy).

[0006] Mitochondrial dysfunction is the main cause of skin wrinkles and chronic inflammation. Similarly, improving mitochondrial function is an important target for combating skin wrinkles and inhibiting chronic inflammation. Currently, the drugs on the market for improving mitochondrial function mainly include PQQ, NMN, metformin, coenzyme Q10, and MitoQ. Among them, PQQ, coenzyme Q10, and MitoQ mainly improve mitochondrial function, anti-oxidation, and anti-aging effects by scavenging free radicals. In addition, the limitation of MitoQ is that it is toxic to nerve cells; NMN mainly increases NAD +The content of coenzymes improves mitochondrial function; metformin repairs mitochondrial function by enhancing autophagy, but its drug cost is relatively high and is not suitable for large-scale production and application; therefore, the development of anti-wrinkle active peptides and anti-inflammatory active peptide products targeting mitochondrial targets has great significance and market prospects. Summary of the invention

[0007] The purpose of the present invention is to provide an application of the active peptide SA-LFP in the preparation of products for improving mitochondrial function and anti-wrinkle and anti-inflammatory products. The specific sequence of the active peptide SA-LFP involved in the present invention is SEQ ID NO 1: CLAGRRRRSV. Studies in CN117024518A show that the SA-LFP active peptide designed and screened based on AI has excellent antioxidant properties and repair effects. The present invention further studies and experiments to prove that the active peptide SA-LFP can promote mitochondrial biogenesis by activating PGC-1ɑ and regulate related metabolic pathways; and activate SIRTs gene and collagen expression, and inhibit MFN1 gene and SASP expression, thereby improving mitochondrial function and achieving anti-wrinkle and anti-inflammatory effects.

[0008] In order to achieve the above-mentioned purpose, the present invention provides an application of an active polypeptide in the preparation of a product for improving mitochondrial function, wherein the active polypeptide is an active polypeptide SA-LFP with an amino acid sequence of CLAGRRRRSV, or a derivative palmitoylated-modified SA-LFP active peptide, an acetyl-modified SA-LFP active peptide, a cyclized SA-LFP active peptide, or a biotin-modified SA-LFP active peptide.

[0009] Preferably, the active peptide is added to the product in an amount of 1-1000 ppm.

[0010] The present invention further provides an application of an active polypeptide SA-LFP in the preparation of an anti-wrinkle product, wherein the active polypeptide is an active polypeptide SA-LFP with an amino acid sequence of CLAGRRRRSV, or a derivative palmitoylated-modified SA-LFP active peptide, an acetyl-modified SA-LFP active peptide, a cyclized SA-LFP active peptide, or a biotin-modified SA-LFP active peptide.

[0011] Specifically, it activates the expression of PGC-1ɑ, a key regulatory factor in mitochondria, thereby promoting SIRTs activity and activating collagen gene expression to achieve firming and anti-wrinkle effects.

[0012] More specifically, the active peptide is added to the product in an amount of 1-1000 ppm.

[0013] The present invention provides an application of an active polypeptide SA-LFP in the preparation of an anti-inflammatory product. The active polypeptide is an active polypeptide SA-LFP with an amino acid sequence of CLAGRRRRSV, or a derivative palmitoylated modified SA-LFP active peptide, an acetyl modified SA-LFP active peptide, a cyclized SA-LFP active peptide, or a biotin modified SA-LFP active peptide.

[0014] Specifically, it achieves anti-inflammatory effects by activating the expression of PGC-1ɑ, a key mitochondrial regulatory factor, thereby reducing the expression of MFN1 gene and the expression of IL-6 and TNFɑ proteins.

[0015] More specifically, the active peptide is added to the product in an amount of 1-1000 ppm.

[0016] The product is food, medicine, health care product, or food additive, health care product additive.

[0017] The present invention relates to a new application of active peptides in improving mitochondrial function and anti-wrinkle and anti-inflammatory. The active peptides take mitochondria as the action target and can achieve anti-wrinkle and anti-inflammatory activity by regulating and improving mitochondrial function. BRIEF DESCRIPTION OF THE DRAWINGS

[0018] Figure 1 Diagram of the mitochondrial regulatory network.

[0019] Figure 2 Show the effect of SA-LFP on the expression of PGC-1α, MFN1, Sirt3, and Sirt4.

[0020] Figure 3 Showing SA-LFP to NAD + Content, NAD + / The effect of NADH.

[0021] Figure 4 Shown is the effect of SA-LFP on mitochondrial membrane potential.

[0022] Figure 5 Show the effect of SA-LFP on collagen gene expression.

[0023] Figure 6 Show that SA-LFP can restore the zebrafish tail fin area.

[0024] Figure 7 Show the effect of SA-LFP on IL-6 and TNFα proteins.

[0025] Figure 8 Showing the effect of SA-LFP on neutrophils in zebrafish.

[0026] Fig. 9Showing the effects of SA-LFP on human periocular and neck wrinkles and facial erythema. DETAILED DESCRIPTION

[0027] The features and exemplary embodiments of various aspects of the present invention will be described in detail below. The specific embodiments listed in the present invention are only examples of the present invention, and the present invention is not limited to the specific embodiments described below.

[0028] Example 1: SA-LFP can activate PGC-1ɑ / Sirt3, Sirt4 gene expression and inhibit MFN1 gene expression

[0029] 1) Experimental methods

[0030] HaCaT cells were plated in a 6-well plate at a density of 1.0×10^5 cells / mL. After the cells were cultured for 24 hours and stabilized, 85 mM AAPH was added to the model group and the experimental group for 2 hours, and then the culture medium was discarded. The experimental group was added with culture medium containing different concentrations of SA-LFP (1, 10, 100 ug / mL), and the blank control group and the model group were added with complete culture medium. The cells were incubated at 37°C and 5% CO. 2 Continue to culture for 24 hours. Obtain RNA solution according to the DP451 kit and store at -80°C for later use. Take a certain amount of RNA extract and use RNase-Free ddH 2 Dilute 5-fold with RNase-Free ddHO. 2 O Zero the spectrophotometer and take the dilution to measure OD 260 OD 280The RNA concentration was determined according to the following formula. Then the PCR reaction was performed according to the TAKARA-qPCRCN830A kit, and the experiment was repeated 3 times. The primers designed for this experiment were PGC-1ɑ: 5′-AGTCCCTGCTCG AATCTTCCT-3′ (forward) and 5′-TCCCAAGGCAGAACAGATATACC-3′ (reverse), MFN1: 5′-GGTGAATGAGCGGCTTTCCAAG-3′ (forward) and 5′-TCCTCCACCAAGAAATGCAGGC-3′ (reverse), Sirt3: 5′-CCCTGGAAACTACAAGCCCAAC-3′ (forward) and 5′-GCAGAGGCAAAGGTT CCATGAG-3′ (reverse), Sirt4: 5′-GTGGATGCTTTGCACACCAAGG-3′ (forward) and 5′-GGTTC AGGACTTGGAAACGCTC-3′ (reverse), and GAPDH: 5′-CATGAGAAGTATGACAACAGCCT-3′ (forward) and 5′-AGTCCTTCCACGATACCAAAGT-3′ (reverse).

[0031] 2) Experimental results:

[0032] Previous studies have shown that PGC-1ɑ is a key regulator of mitochondrial function. Figure 2 As shown, compared with the blank control group, when the cells were damaged by the inducer AAPH, the expression of PGC-1ɑ was significantly reduced, and when the cells were further acted on by SA-LFP, the gene expression of PGC-1ɑ was significantly increased, and at the same time, the gene expression levels of PGC-1ɑ's downstream proteins Sirt3 and Sirt4 were also significantly increased, while the gene expression level of MFN1 was significantly decreased, indicating that SA-LFP can activate PGC-1ɑ and inhibit the expression of MFN1, and at the same time promote the expression of Sirt3 and Sirt4.

[0033] Example 2: SA-LFP can increase NAD + Content and increase NAD + / NADH

[0034] 1) Experimental methods

[0035] HaCaT cells were plated in a 6-well plate at a density of 1.0×10^5 cells / mL. After the cells were cultured for 24 hours and stabilized, 85 mM AAPH was added to the model group and the experimental group for 2 hours, and then the culture medium was discarded. The experimental group was added with culture medium containing different concentrations of SA-LFP (1, 10, 100 ug / mL), and the blank control group and the model group were added with complete culture medium. The cells were incubated at 37°C and 5% CO.2 Continue to culture for 24 hours. Extract total cell protein according to the S0175 kit. Then obtain a standard curve according to the kit. + , NADH content was tested, and NAD was calculated based on the test results. + Content and NAD + / NADH ratio, and the experiment was repeated 3 times.

[0036] 2) Experimental results

[0037] NAD + With NAD + / NADH plays an important role in mitochondrial energy metabolism, redox balance, signal transduction, metabolic regulation, and stress response, and is a key factor in maintaining cell health and mitochondrial function. + It is also the main substrate of Sirts protein, directly affecting the expression level of Sirts protein. Figure 3 The results showed that when AAPH was used to treat cells, NAD + However, with the increase of SA-LFP concentration, NAD + The content increased in a concentration-dependent manner, and NAD + The / NADH ratio also increased with the increase of SA-LFP concentration, indicating that SA-LFP can increase NAD + The content promotes mitochondrial energy metabolism.

[0038] Example 3: SA-LFP can restore mitochondrial membrane potential and improve mitochondrial function

[0039] 1) Experimental methods

[0040] HaCaT cells were plated in a 6-well plate at a density of 1.0×10^5 cells / mL. After the cells were cultured for 24 hours and stabilized, 85 mM AAPH was added to the model group and the experimental group for 2 hours, and then the culture medium was discarded. The experimental group was added with culture medium containing different concentrations of SA-LFP (1, 10, 100 ug / mL), and the blank control group and the model group were added with complete culture medium. The cells were incubated at 37°C and 5% CO. 2 Continue to culture for 24 hours. According to the E-CK-A301 kit, discard the culture supernatant and wash the cells once with 1×JC-1Assay Buffer. Add 1mL JC-1 working solution and incubate at 37℃ for 20min. After the incubation, wash the cells once with 1×JC-1Assay Buffer, then add 2mL cell culture medium or 1×JC-1Assay Buffer, observe the results under a laser confocal microscope, and repeat the experiment 3 times.

[0041] 2) Experimental results

[0042] Mitochondrial membrane potential reflects the integrity of mitochondrial function and is a sensitive indicator for evaluating mitochondrial function. The stability of mitochondrial membrane potential is conducive to maintaining the normal physiological function of cells. In normal mitochondria, JC-1 aggregates in the mitochondrial matrix and emits strong red fluorescence; when the mitochondrial membrane potential decreases or is lost, JC-1 can only exist in the cytoplasm in the form of monomers, emitting green fluorescence. Figure 4 As shown. Compared with the blank group, after AAPH acted on the cells, the cells emitted green fluorescence, indicating that the mitochondria were damaged, the membrane potential decreased, the mitochondrial homeostasis of the cells was disturbed, and the activity decreased. Compared with the AAPH group, the red fluorescence of the SA-LFP experimental group was significantly enhanced, the mitochondrial membrane potential increased, and the mitochondria recovered their vitality, indicating that SA-LFP can restore the mitochondrial membrane potential. In summary, SA-LFP can activate PGC-1ɑ and further improve mitochondrial function and enhance mitochondrial vitality.

[0043] Example 4: SA-LFP can promote collagen gene expression

[0044] 1) Experimental methods

[0045] Healthy adult zebrafish were selected, and normal control group and SA-LFP experimental group were set up, with 30 fish in each group. Water-soluble samples were given, and the volume of each well was 3mL. Three biological replicates were performed. Incubate at 28℃ in the dark for 24h. Total RNA of zebrafish in each experimental group was extracted, cDNA was synthesized, and q-PCR was used to detect the gene expression of β-actin and target gene. β-actin was used as the internal reference of gene expression to calculate the relative RNA expression of target gene.

[0046] 2) Experimental results

[0047] Type I collagen is a trimer, mainly composed of two ɑ1 chains and one ɑ2 chain, encoded by col1ɑ1ɑ and col1ɑ2 genes, respectively. It performs collagen-related biological functions in connective tissue and bone and is the main component of ECM. There are three type I collagen genes in zebrafish, col1ɑ1ɑ, col1ɑ1b and col1ɑ2, which encode the ɑ1(I), ɑ2(I) and ɑ3(I) chains respectively. Figure 5 As shown in the figure, the relative expression of col1a1a gene in the SA-LFP group was significantly increased compared with the normal control group, indicating that SA-LFP can promote the expression of collagen genes.

[0048] Example 5: SA-LFP has significant anti-wrinkle activity

[0049] 1) Experimental methods

[0050] Healthy adult zebrafish were selected, and a normal control group, SA-LFP sample group, and model control group were set up, with 15 fish in each group. 0.01% SA-LFP was given in water, and the capacity of each well was 3 mL. Three biological replicates were performed. Incubate in the dark at 28°C for 2 hours. Except for the normal control group, the zebrafish in the other experimental groups were irradiated under ultraviolet light three times, each irradiation time was 15 minutes, and the interval was 30 minutes. Continue to incubate in the dark at 28°C for 22 hours. Ten zebrafish were randomly selected from each experimental group and photographed under a dissecting microscope. Advanced image processing software was used to analyze and collect data, and the zebrafish tail fin area (A) was analyzed. According to the formula, it was calculated and judged whether the sample had anti-wrinkle effect. The calculation formula is as follows: Anti-wrinkle effect (%) = [A (sample group) - A (model control group)] / [A (normal control group) - A (model control group)] * 100%

[0051] 2) Experimental results

[0052] The structure of zebrafish skin is similar to that of human skin. When exposed to excessive ultraviolet rays, it can lead to a decrease in collagen and elastin in the skin, which manifests as wrinkling of the tail fin skin. Compared with the model control group, the tail fin area of ​​zebrafish in the SA-LFP group increased significantly by 27%, indicating that SA-LFP has significant anti-wrinkle activity. Figure 6 )

[0053] Example 6: SA-LFP can inhibit the expression of SASP (IL-6, TNFɑ) proteins

[0054] 1) Experimental methods

[0055] Raw264.7 cells were seeded on a 96-well plate at a density of 5X10^5 cells / mL. When the cells grew to about 80% of the total volume, PBS was added to the blank control group. In the drug-treated group, 1ug / mL LPS was added and mixed with peptides of different concentrations. After addition, the cells were kept at 37°C and 5% CO. 2 Incubate in the incubator for 24 hours. After the incubation, collect the cell culture fluid to obtain the sample fluid, and operate according to the IL-6 and TNFα ELISA operating instructions. Use a microplate reader to measure the OD value of each well at 450nm within 15 minutes, and repeat the experiment 3 times.

[0056] 2) Experimental results

[0057] Lipopolysaccharide (LPS) binds to cell surface receptors, activates inflammatory cytokine gene expression and causes an inflammatory response, and then the cells secrete a series of proinflammatory factors, which is also called the senescence-associated secretory phenotype (SASP). Studies have shown that inhibiting MFN1 can reduce SASP, and the present invention also confirms that SA-LFP can inhibit MFN1. Therefore, this experiment uses 10ug / mL SA-LFP to treat the LPS-induced inflammatory cell model and detect the IL-6 and TNFɑ content in the corresponding cells to determine whether the bioactive peptide of the present invention can inhibit the expression of SASP (IL-6, TNFɑ). The results are as follows: Figure 7 As shown, compared with the blank control group, the concentrations of IL-6 and TNFɑ in the PBS group were significantly increased, indicating that the inflammatory model was successfully induced, and the content of inflammatory factors decreased significantly after SA-LFP acted on the cells, with the reduction rate of IL-6 reaching 25% (P<0.001) and the reduction rate of TNFɑ reaching 13% (P<0.001), indicating that SA-LFP can significantly reduce the expression of inflammatory factors IL-6 and TNFɑ, and has excellent anti-inflammatory effects.

[0058] Example 7: SA-LFP can reduce the neutrophil content in zebrafish

[0059] 1) Experimental methods

[0060] Healthy adult zebrafish were selected, and a normal control group, SA-LFP sample group, and model control group were set up, with 15 fish in each group. SLS was given in water to establish a zebrafish skin inflammation model, and 0.002% SA-LFP was given to the sample group, with a capacity of 3 mL per well. Three biological replicates were performed. Incubate in the dark at 28°C for 18 hours. Ten zebrafish were randomly selected from each experimental group and photographed under a fluorescence microscope. Advanced image processing software was used to analyze and collect data, and the number of neutrophils in the zebrafish skin (N) was analyzed. The formula was used to calculate and determine whether the sample had anti-inflammatory and soothing effects. The calculation formula is as follows: Anti-inflammatory and soothing effect (%) = [N (model control group) - N (sample group)] / [N (model control group) - N (normal control group)] * 100%

[0061] 2) Experimental results

[0062] Sodium dodecyl sulfate (SLS) may cause irritation in the body after acting on it. The irritant enters the zebrafish body, induces an inflammatory response, and neutrophils have an immune response, migrating to the skin epidermis and gathering. It was observed that the number of neutrophils in the SA-LFP group was significantly reduced compared with the model control group. The reduction rate calculated by the formula was 19%, indicating that SA-LFP has anti-inflammatory and soothing effects. ( Figure 8 )

[0063] Example 8: Human trials show that SA-LFP has anti-wrinkle and soothing effects

[0064] 1) Experimental methods

[0065] A total of 65 volunteers were recruited in this experiment, including 33 in the matrix group and 32 in the SA-LFP group. The method of self-control before and after and placebo control was adopted. The anti-wrinkle, firming and soothing effects of SA-LFP were evaluated by photographing the changes in dermal thickness, dermal density, periocular wrinkles and the number, length and depth of neck wrinkles on the 0th and 28th days after use of the volunteers and measuring the changes in skin erythema index.

[0066] 2) Experimental results

[0067] The results are as follows Fig. 9 As shown in the figure, after the volunteers used SA-LFP for 28 days continuously, the dermal thickness and skin smoothness of the volunteers' skin were significantly improved, as shown in Figures a and b. As shown in Figures c and f, the number, length and depth of wrinkles around the eyes of the volunteers were significantly improved, and compared with the matrix group, the number of wrinkles decreased by 2.5 times (P<0.001), and the neck wrinkles also showed significant improvement accordingly. As shown in Figure e, the area of ​​facial erythema of the volunteers was significantly reduced, while there was no significant change in the matrix group. The results showed that SA-LFP can significantly increase the thickness of the dermis, improve the smoothness of the skin, and show a significant firming effect; it can also significantly improve the wrinkles around the eyes and neck, reduce the number of wrinkles, and have a significant anti-wrinkle effect. It can also improve skin redness and have a soothing effect. In summary, SA-LFP has a significant anti-wrinkle and soothing effect.

Claims

1. Use of an active polypeptide in preparing a product for improving mitochondrial function, characterized in that: The active polypeptide is the active polypeptide SA-LFP with an amino acid sequence of CLAGRRRRSV, or a derivative palmitoylated modified SA-LFP active peptide, an acetyl modified SA-LFP active peptide, a cyclized SA-LFP active peptide, or a biotin modified SA-LFP active peptide.

2. The use according to claim 2, characterized in that The active peptide is added to the product in an amount of 1-1000 ppm.

3. An application of an active polypeptide SA-LFP in the preparation of anti-wrinkle products, characterized in that: The active polypeptide is the active polypeptide SA-LFP with an amino acid sequence of CLAGRRRRSV, or a derivative palmitoylated modified SA-LFP active peptide, an acetyl modified SA-LFP active peptide, a cyclized SA-LFP active peptide, or a biotin modified SA-LFP active peptide.

4. The use according to claim 3, characterized in that It activates the expression of PGC-1ɑ, a key regulatory factor in mitochondria, thereby promoting SIRTs activity and activating collagen gene expression to achieve firming and anti-wrinkle effects.

5. The use according to claim 3 or 4, characterized in that The active peptide is added to the product in an amount of 1-1000 ppm.

6. The use according to claim 3 or 4, characterized in that The product is food, medicine, health care product, or food additive, health care product additive.

7. Use of an active polypeptide SA-LFP in the preparation of an anti-inflammatory product, characterized in that: The active polypeptide is the active polypeptide SA-LFP with an amino acid sequence of CLAGRRRRSV, or a derivative palmitoylated modified SA-LFP active peptide, an acetyl modified SA-LFP active peptide, a cyclized SA-LFP active peptide, or a biotin modified SA-LFP active peptide.

8. The use according to claim 7, characterized in that It achieves anti-inflammatory effects by inhibiting the expression of MFN1 gene and the expression of IL-6 and TNFɑ proteins.

9. The use according to claim 7 or 8, characterized in that The active peptide is added to the product in an amount of 1-1000 ppm.

10. The use according to claim 7 or 8, characterized in that: The product is food, medicine, health care product, or food additive, health care product additive.

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